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Articles de revues sur le sujet « Endothelin Axi »

Auteur : Grafiati

Publié le 9 mars 2023

Mis à jour le 31 juillet 2025

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1

Tyagi, Suresh C., Lane M. Smiley, and Vibhas S. Mujumdar. "Homocyst(e)ine impairs endocardial endothelial function." Canadian Journal of Physiology and Pharmacology 77, no. 12 (1999): 950–57. http://dx.doi.org/10.1139/y99-102.

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Homocyst(e)ine injured vascular endothelium and modulated endothelial-dependent vascular function. Endothelium plays an analogous role in both the vessel and the endocardium. Therefore, we hypothesized that homocyst(e)ine modulated endocardial endothelium (EE) dependent cardiac function. The ex vivo cardiac rings from normal male Wistar-Kyoto rats were prepared. The contractile responses of left and right ventricular rings were measured in an isometric myobath, using different concentrations of CaCl2. The response was higher in the left ventricle than right ventricle and was elevated in endoca

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O. R. Luchko. "A relation of the indices of systemic inflammation and endothelial dysfunction in patients with chronic pyelonephritis and arterial hypertension." Bukovinian Medical Herald 17, no. 1 (65) (2013): 59–63. http://dx.doi.org/10.24061/2413-0737.xvii.1.65.2013.15.

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The dynamics of the indicators of systemic inflammation (C-reactive protein - CRP, tumor necrosis factoralpha – TNF-α, IL-1 – IL-1, IL-6 – IL-6, soluble cell-cell adhesion molecule – sICAM-1) and endothelial dysfunction (pulse blood pressure – PBP, aortic stiffness index – ASI, the thickness of intima-media complex – TIMC, the velocity of the pulse wave propagation – VPWP, CAVI, endothelium dependent vasodilatation – EDVD and endothelium independent vasodilatation – EIVD, endothelin-1 – ET-1) in 105 patients with chronic pyelonephritis (CPN) and arterial hypertension (AH), depending on the glo

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Hao, Ying, Zhuang Wang, Francis Frimpong, and Xingjuan Chen. "Calcium–Permeable Channels and Endothelial Dysfunction in Acute Lung Injury." Current Issues in Molecular Biology 44, no. 5 (2022): 2217–29. http://dx.doi.org/10.3390/cimb44050150.

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The increased permeability of the lung microvascular endothelium is one critical initiation of acute lung injury (ALI). The disruption of vascular-endothelium integrity results in leakiness of the endothelial barrier and accumulation of protein-rich fluid in the alveoli. During ALI, increased endothelial-cell (EC) permeability is always companied by high frequency and amplitude of cytosolic Ca2+ oscillations. Mechanistically, cytosolic calcium oscillations include calcium release from internal stores and calcium entry via channels located in the cell membrane. Recently, numerous publications h

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Lam, Chen-Fuh, Yen-Chin Liu, Jen-Kuo Hsu, et al. "Autologous Transplantation of Endothelial Progenitor Cells Attenuates Acute Lung Injury in Rabbits." Anesthesiology 108, no. 3 (2008): 392–401. http://dx.doi.org/10.1097/aln.0b013e318164ca64.

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Background Acute lung injury (ALI) and end-stage acute respiratory distress syndrome (ARDS) are among the most common causes of death in intensive care units. Activation and damage of pulmonary endothelium is the hallmark of ALI/ARDS. Recent studies have demonstrated the importance of circulating endothelial progenitor cells (EPCs) in maintaining normal endothelial function as well as endothelial repairing after vascular injury. Here, the authors present the first study demonstrating the therapeutic potential of EPCs in a rabbit model of ALI/ARDS. Methods Circulating EPCs were obtained from ra

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Vorob’eva, Nadezda A., Alena I. Vorob’eva, and Anastasiya A. Marusiy. "Risk of Endothelial Dysfunction and Total Antioxidant Capacity in Seafarers During an Arctic Voyage." Journal of Medical and Biological Research, no. 2 (May 9, 2021): 192–200. http://dx.doi.org/10.37482/2687-1491-z057.

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Among other areas of research, clinical medicine studies the adaptation mechanisms of the vascular endothelium to the extreme conditions of the Arctic. This paper dwells on the possible relationship of the development of endothelial dysfunction and the antioxidant system with modifiable risk factors during a short translatitudinal voyage in the Arctic. The study involved 32 crew members of the research vessel Mikhail Somov during the TransArctic–2019 research expedition. Venous blood sampling was carried out before the voyage at the zero point (Arkhangelsk, 64°33’N 40°32’E) and at the highest

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Mejía-Salgado, Germán, Paula Tatiana Muñoz-Vargas, Carlos Cifuentes-González, et al. "Quantitative changes in the corneal endothelium and central corneal thickness during anterior chamber inflammation: A systematic review and meta-analysis." PLOS ONE 19, no. 1 (2024): e0296784. http://dx.doi.org/10.1371/journal.pone.0296784.

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Purpose To establish the effects of anterior chamber inflammation (ACI) on the corneal endothelium parameters and central corneal thickness (CCT). Methods We conducted a comprehensive literature review using medical databases (PubMed, EMBASE, VHL, and medRxiv) on March 8, 2023, for studies that included patients with ACI who had undergone specular microscopy or pachymetry. Case series with >10 patients, cross-sectional, case-control, and cohort studies were included. The risk of bias was assessed using CLARITY tools and validated scales such as those by Hassan Murad et al. and Hoy et al. A

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Zaikina, T. S., P. G. Kravchun, D. V. Minukhina, D. V. Minukhin, D. O. Yevtushenko, and I. O. Kudrevych. "COMPREHENSIVE ASSESSMENT OF ENDOTHELIUM-DEPENDENT MEDIATORS IN PATIENTS WITH ACUTE MYOCARDIAL INFARCTION AND DIABETES MELLITUS TYPE 2." Problems of Endocrine Pathology 76, no. 2 (2021): 14–18. http://dx.doi.org/10.21856/j-pep.2021.2.02.

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The aim of study is to evaluate the levels of endothelium-dependent mediators: endothelial nitric-oxide synthase (NOS), plasminogen activator inhibitor-1 (PAI-1) and circulating soluble CD40 ligand (sCD40L) in patients with acute myocardial infarction (AMI) and concomitant type 2 diabetes mellitus (DM). The study included 255 patients with AMI, who were divided into two groups depending on the presence of concomitant type 2 DM: 1 group — 143 patients with concomitant type 2 DM; 2 group — 112 patients without concomitant disturbances of carbohydrate metabolism. Studied endothelial-dependent ind

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Wang, Fei, Hui Zhang, Kotaro Uchida, et al. "The Evaluation Value of Non-Invasive Indices of Arterial Stiffness in the Early Stage of Coronary Artery Disease: Preliminary Results from an Exploratory Study." Journal of Vascular Diseases 3, no. 3 (2024): 278–89. http://dx.doi.org/10.3390/jvd3030022.

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Background: Recently, the arterial velocity pulse index (AVI) and arterial pressure volume index (API) have been used to evaluate arterial stiffness and endothelial function. As arterial stiffness and endothelial injury are risk factors for coronary artery disease (CAD), these two indexes are therefore expected to predict and evaluate the future risk of CAD and cardiovascular events before clinical manifestations. Methods: A total of 90 consecutive patients with coronary angiography (CAG) were enrolled. After excluding normal patients and acute coronary syndrome patients, forty-seven patients

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Kolosova, Irina A., Tamara Mirzapoiazova, Liliana Moreno-Vinasco, Saad Sammani, Joe G. N. Garcia та Alexander D. Verin. "Protective effect of purinergic agonist ATPγS against acute lung injury". American Journal of Physiology-Lung Cellular and Molecular Physiology 294, № 2 (2008): L319—L324. http://dx.doi.org/10.1152/ajplung.00283.2007.

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Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are major causes of acute respiratory failure associated with high morbidity and mortality. Although ALI/ARDS pathogenesis is only partly understood, pulmonary endothelium plays a major role by regulating lung fluid balance and pulmonary edema formation. Consequently, endothelium-targeted therapies may have beneficial effects in ALI/ARDS. Recently, attention has been given to the therapeutic potential of purinergic agonists and antagonists for the treatment of cardiovascular and pulmonary diseases. Extracellular purines (ad

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Dube, Shataakshi, Tejasvi Matam, Jessica Yen, et al. "Endothelial STAT3 Modulates Protective Mechanisms in a Mouse Ischemia-Reperfusion Model of Acute Kidney Injury." Journal of Immunology Research 2017 (2017): 1–9. http://dx.doi.org/10.1155/2017/4609502.

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STAT3 is a transcriptional regulator that plays an important role in coordinating inflammation and immunity. In addition, there is a growing appreciation of the role STAT3 signaling plays in response to organ injury following diverse insults. Acute kidney injury (AKI) from ischemia-reperfusion injury is a common clinical entity with devastating consequences, and the recognition that endothelial alterations contribute to kidney dysfunction in this setting is of growing interest. Consequently, we used a mouse with a genetic deletion of Stat3 restricted to the endothelium to examine the role of S

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Gauthier, Kathryn M., David X. Zhang, Erik M. Edwards, Blythe Holmes, and William B. Campbell. "Angiotensin II Dilates Bovine Adrenal Cortical Arterioles: Role of Endothelial Nitric Oxide." Endocrinology 146, no. 8 (2005): 3319–24. http://dx.doi.org/10.1210/en.2005-0129.

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Abstract Adrenal steroidogenesis is modulated by humoral and neuronal factors and blood flow. Angiotensin II (AII) stimulates adrenal cortical aldosterone and cortisol production and medullary catecholamine release. However, AII regulation of adrenal vascular tone has not been characterized. We examined the effect of AII on diameters of cannulated bovine adrenal cortical arteries. Cortical arteries (average internal diameter = 230 μm) were constricted with U46619 and concentration-diameter responses to AII (10−13 to 10−8 mol/liter) were measured. In endothelium-intact arteries, AII induced dil

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Stanojevic, Dragana, Svetlana Apostolovic, Sonja Salinger-Martinovic, et al. "Endothelin-1 and nitric oxide in 3-year prognosis after acute myocardial infarction." Vojnosanitetski pregled 74, no. 9 (2017): 862–70. http://dx.doi.org/10.2298/vsp151029278s.

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Background/Aim. Acute myocardial infarction (AMI) is an important cause of mortality/morbidity worldwide. Biomarkers improve diagnostic and prognostic accuracy in AMI. The aim of this study was to investigate an increase of markers of endothelial dysfunction in AMI, measured on the 3rd day after the initial event and to investigate their association with short- and long-term (3-year) prognosis (outcome). Methods. The prospective study included 108 patients with AMI in the experimental group and 50 apparently healthy subjects in the control group. Endothelin-1 (ET-1) and nitric oxide degradatio

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Димова, Евгения, and Evgeniya Dimova. "THE STATE OF VASOMOTOR ENDOTHELIAL FUNCTION IN PATIENTS WITH CHRONIC OBSTRUCTIVE PULMONARY DISEASE IN COMBINATION WITH ACUTE MYOCARDIAL INFARCTION." Bulletin physiology and pathology of respiration 1, no. 67 (2018): 37–40. http://dx.doi.org/10.12737/article_5a9f261dc23047.85257701.

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The aim of the study is to investigate a vasomotor function of patients with COPD against the development of acute myocardial infarction (AMI) with an elevation of the ST segment of the electrocardiogram. The brachial artery reactivity was studied in 42 patients with COPD during the course of treatment in the Amur Regional Clinical Hospital. All the patients were divided into two groups: 1st group (22 patients) with COPD and AMI with an elevation of the ST segment; 2nd group (20 patients) - with moderate COPD. The control group included 15 healthy people without cardiovascular diseases and res

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Htwe, Yu Maw, Huashan Wang, Patrick Belvitch, et al. "Group V Phospholipase A2 Mediates Endothelial Dysfunction and Acute Lung Injury Caused by Methicillin-Resistant Staphylococcus aureus." Cells 10, no. 7 (2021): 1731. http://dx.doi.org/10.3390/cells10071731.

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Lung endothelial dysfunction is a key feature of acute lung injury (ALI) and clinical acute respiratory distress syndrome (ARDS). Previous studies have identified the lipid-generating enzyme, group V phospholipase A2 (gVPLA2), as a mediator of lung endothelial barrier disruption and inflammation. The current study aimed to determine the role of gVPLA2 in mediating lung endothelial responses to methicillin-resistant Staphylococcus aureus (MRSA, USA300 strain), a major cause of ALI/ARDS. In vitro studies assessed the effects of gVPLA2 inhibition on lung endothelial cell (EC) permeability after e

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Chiba, Takuto, Débora M. Cerqueira, Yao Li, et al. "Endothelial-Derived miR-17∼92 Promotes Angiogenesis to Protect against Renal Ischemia-Reperfusion Injury." Journal of the American Society of Nephrology 32, no. 3 (2021): 553–62. http://dx.doi.org/10.1681/asn.2020050717.

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BackgroundDamage to the renal microvasculature is a hallmark of renal ischemia-reperfusion injury (IRI)–mediated AKI. The miR-17∼92 miRNA cluster (encoding miR-17, -18a, -19a, -20a, -19b-1, and -92a-1) regulates angiogenesis in multiple settings, but no definitive role in renal endothelium during AKI pathogenesis has been established.MethodsAntibodies bound to magnetic beads were utilized to selectively enrich for renal endothelial cells from mice. Endothelial-specific miR-17∼92 knockout (miR-17∼92endo−/−) mice were generated and given renal IRI. Mice were monitored for the development of AKI

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Christofidou-Solomidou, Melpo, Arnaud Scherpereel, Rainer Wiewrodt, et al. "PECAM-directed delivery of catalase to endothelium protects against pulmonary vascular oxidative stress." American Journal of Physiology-Lung Cellular and Molecular Physiology 285, no. 2 (2003): L283—L292. http://dx.doi.org/10.1152/ajplung.00021.2003.

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Targeted delivery of drugs to vascular endothelium promises more effective and specific therapies in many disease conditions, including acute lung injury (ALI). This study evaluates the therapeutic effect of drug targeting to PECAM (platelet/endothelial cell adhesion molecule-1) in vivo in the context of pulmonary oxidative stress. Endothelial injury by reactive oxygen species (e.g., H2O2) is involved in many disease conditions, including ALI/acute respiratory distress syndrome and ischemia-reperfusion. To optimize delivery of antioxidant therapeutics, we conjugated catalase with PECAM antibod

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Maakaron, Joseph, Emily Stene, Megan Bruns, et al. "Icans Prophylaxis with Simvastatin and Intrathecal Dexamethasone in Adults Receiving Axicabtagene Ciloleucel (Axi-Cel) Treatment." Blood 138, Supplement 1 (2021): 1744. http://dx.doi.org/10.1182/blood-2021-149607.

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Abstract Background Axi-cel is approved for the treatment of relapsed/refractory diffuse large B-cell lymphoma since 2017 and has demonstrated efficacy and durability but with significant side effects, namely cytokine release syndrome (CRS) and neurotoxicity (ICANS). In patients receiving axi-cel for aggressive lymphomas, any grade ICANS occurs at a rate of 50% and grade 3/4 occurs about 35% of the time. The mechanism underlying ICANS remains unclear. The current working hypothesis is that endothelial injury caused by the disease and lymphodepleting chemotherapy leads to breakdown of the blood

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Rajendran, Ganeshkumar, Michael P. Schonfeld, Ratnakar Tiwari, et al. "Inhibition of Endothelial PHD2 Suppresses Post-Ischemic Kidney Inflammation through Hypoxia-Inducible Factor-1." Journal of the American Society of Nephrology 31, no. 3 (2020): 501–16. http://dx.doi.org/10.1681/asn.2019050523.

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BackgroundProlyl-4-hydroxylase domain-containing proteins 1–3 (PHD1 to PHD3) regulate the activity of the hypoxia-inducible factors (HIFs) HIF-1 and HIF-2, transcription factors that are key regulators of hypoxic vascular responses. We previously reported that deficiency of endothelial HIF-2 exacerbated renal ischemia-reperfusion injury, whereas inactivation of endothelial PHD2, the main oxygen sensor, provided renoprotection. Nevertheless, the molecular mechanisms by which endothelial PHD2 dictates AKI outcomes remain undefined.MethodsTo investigate the function of the endothelial PHD2/HIF ax

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Ryabov, V. V., S. V. Popov, E. V. Vyshlov, et al. "Reperfusion cardiac injury. The role of microvascular obstruction." Siberian Journal of Clinical and Experimental Medicine 38, no. 2 (2023): 14–22. http://dx.doi.org/10.29001/2073-8552-2023-39-2-14-22.

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Microvascular obstruction (MVO) of coronary arteries increases the mortality rate and major adverse cardiac events in patients with acute myocardial infarction (AMI) and percutaneous coronary intervention (PCI). According to preliminary data platelets, inflammation, Ca2+ overload, neuropeptide Y, and endothelin-1 could be involved in the pathogenesis of MVO. Many questions related to the pathogenesis of MVO remain unanswered. The role of endothelial cell damage in the formation of MVO in patients with AMI and PCI is unknown. It is unclear whether nitric oxide (NO) production reduces or decreas

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Hartopo, Anggoro Budi, and Lucia Kris Dinarti. "The Shared Pathogenesis of Pulmonary Artery Hypertension." ACI (Acta Cardiologia Indonesiana) 4, no. 1 (2018): 22. http://dx.doi.org/10.22146/aci.36635.

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Pulmonary artery hypertension is defined as an increased in pulmonary artery pressureexceeding 25 mmHg with normal pulmonary wedge pressure. The pathogenesis of pulmonaryartery hypertension involves interaction among vascular, cellular and biomarker componentsin the pulmonary tissue; with eventual result is elevated pulmonary artery pressure. Vascularcomponents are remodeling of intimal, medial and adventitial layers. Cellular components areplayed by apoptosis-resistant endothelial cells, proliferative-prone pulmonary artery smoothmuscle cells, fibroblasts and inflammatory cells. The functiona

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Yin, Xiuru, Zuodi Liang, Yue Yun, and Ling Pei. "Intravenous Transplantation of BMP2-Transduced Endothelial Progenitor Cells Attenuates Lipopolysaccharide-Induced Acute Lung Injury in Rats." Cellular Physiology and Biochemistry 35, no. 6 (2015): 2149–58. http://dx.doi.org/10.1159/000374020.

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Background/Aims: Acute lung injury (ALI) and its aggressive stage, acute respiratory distress syndrome (ARDS), are characterized by diffuse damage and increased permeability of the endothelial barrier, leading to alveolar infiltrates and interstitial edema. Enhancing endothelial integrity represents a novel therapeutic strategy for ALI/ARDS. Endothelial progenitor cells (EPCs) have been reported to participate in endothelial repair of ALI and also serve as a tool for gene therapy. Further, bone morphogenetic protein 2 (BMP2) is an essential signaling molecule that regulates the fate of differe

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Agneskirchner, Jens, Patrick Bode, Michael Spannagl, Laurenz Wurzinger, and Armin Reininger. "c7E3 Fab Inhibits Low Shear Flow Modulated Platelet Adhesion to Endothelium and Surface-adsorbed Fibrinogen by Blocking Platelet GP IIb/IIIa as well as Endothelial Vitronectin Receptor." Thrombosis and Haemostasis 83, no. 02 (2000): 217–23. http://dx.doi.org/10.1055/s-0037-1613789.

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SummaryThe c7E3 Fab reduces ischemic complications in patients undergoing high-risk coronary angioplasty or atherectomy. The present study investigated how c7E3 Fab inhibition of the platelet receptor glycoprotein IIb/IIIa and the endothelial vitronectin receptor affected platelet adhesion to endothelium and surface adsorbed fibrinogen under flow conditions.Platelet adhesion was examined using a stagnation point flow device with shear stress and shear rates up to 2.2 dynes/cm2 and 170 s−1, respectively. Ex vivo adhesion was compared between two groups of patients with acute myocardial infarcti

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Agarwal, Neera, Sam P. L. Rice, Hemanth Bolusani, et al. "Metformin Reduces Arterial Stiffness and Improves Endothelial Function in Young Women with Polycystic Ovary Syndrome: A Randomized, Placebo-Controlled, Crossover Trial." Journal of Clinical Endocrinology & Metabolism 95, no. 2 (2010): 722–30. http://dx.doi.org/10.1210/jc.2009-1985.

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Abstract Context: Patients with polycystic ovary syndrome (PCOS) have an increased prevalence of insulin resistance and display subclinical evidence of early cardiovascular disease. Metformin improves insulin sensitivity and circulating markers of cardiovascular risk in patients with PCOS, but it is unclear whether this translates into improvements in vascular function. Objective: Our objective was to evaluate the effects of metformin on arterial stiffness and endothelial function in women with PCOS. Design and Intervention: Thirty women with PCOS were assigned to consecutive 12-wk treatment p

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Marrazzo, Francesco, Stefano Spina, Francesco Zadek, et al. "Protocol of a randomised controlled trial in cardiac surgical patients with endothelial dysfunction aimed to prevent postoperative acute kidney injury by administering nitric oxide gas." BMJ Open 9, no. 7 (2019): e026848. http://dx.doi.org/10.1136/bmjopen-2018-026848.

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IntroductionPostoperative acute kidney injury (AKI) is a common complication in cardiac surgery. Levels of intravascular haemolysis are strongly associated with postoperative AKI and with prolonged (>90 min) use of cardiopulmonary bypass (CPB). Ferrous plasma haemoglobin released into the circulation acts as a scavenger of nitric oxide (NO) produced by endothelial cells. Consequently, the vascular bioavailability of NO is reduced, leading to vasoconstriction and impaired renal function. In patients with cardiovascular risk factors, the endothelium is dysfunctional and cannot replenish the N

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Hanke, Craig J., Blythe B. Holmes, Yafei Xu, Kasem Nithipatikom, and William B. Campbell. "Endothelium-Derived Steroidogenic Factor Enhances Angiotensin II-Stimulated Aldosterone Release by Bovine Zona Glomerulosa Cells." Endocrinology 148, no. 1 (2007): 317–23. http://dx.doi.org/10.1210/en.2006-0884.

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Endothelium-derived steroidogenic factor (EDSF) is an endothelial peptide that stimulates aldosterone release from bovine adrenal zona glomerulosa (ZG) cells. The regulation of aldosterone release by combinations of EDSF and angiotensin II (AII) or EDSF and ACTH was investigated. Endothelial cells (ECs) and EC-conditioned media (ECCM) increased aldosterone release from ZG cells, an activity attributed to EDSF. AII (10−12 to 10−8m) and ACTH (10−12 to 10−9m) also stimulated the release of aldosterone from ZG cells. The stimulation by AII, but not ACTH, was greatly enhanced when ZG cells were coi

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Tuychiev, L. N., M. D. Ahkmedova, I. A. Imamova, N. U. Ibragimova, and S. D. Igamberdieva. "Predisposing factors contributing to the development of renal dysfunction in acute infectious diarrhea associated with hemocolitis (AIDH)." Journal Infectology 12, no. 5 (2021): 123–29. http://dx.doi.org/10.22625/2072-6732-2020-12-5-123-129.

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Outcomes of severe variants of acute infectious diarrhea in children with acute renal injury/failure (ARI/ARF) remain unsatisfactory, and mortality reaches 70% and more. ARI/ ARF therapy requires high material costs, which represent significant burden on health financing systems. It makes us consider AFR as one of the most important medical and social problems.The aim of our study was to investigate predisposing factors contributing to the development of renal dysfunction in acute infectious diarrhea associated with hemocolitis (AIDH), as well as to study the relationship of the developed rena

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Athira, U., Sonia Sonia, Astha Sharma, and Sachit Sharma. "Angiogenesis and Vascular Repair in Acute Kidney Injury." Journal for Research in Applied Sciences and Biotechnology 4, no. 2 (2025): 45–54. https://doi.org/10.55544/jrasb.4.2.7.

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Chronic kidney disease (CKD) is one of the most dangerous medical illnesses that can be caused by acute kidney injury (AKI), which is characterised by the sudden cessation of normal kidney function. This condition can also lead to other major complications. Abnormalities of the endothelium, inflammation, and oxidative stress are all factors that contribute to the development of acute kidney injury (AKI), which primarily impacts the vasculature of the kidneys. Renal regeneration is dependent on angiogenesis and vascular repair pathways, which include hypoxia-inducible pathways, vascular endothe

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Mutin, Murielle, Isabelle Canavy, Andrew Blann, Michel Bory, José Sampol, and Françoise Dignat-George. "Direct Evidence of Endothelial Injury in Acute Myocardial Infarction and Unstable Angina by Demonstration of Circulating Endothelial Cells." Blood 93, no. 9 (1999): 2951–58. http://dx.doi.org/10.1182/blood.v93.9.2951.

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Abstract Circulating endothelial cells (CECs) have been detected in association with endothelial injury and therefore represent proof of serious damage to the vascular tree. Our aim was to investigate, using the technique of immunomagnetic separation, whether the pathological events in unstable angina (UA) or acute myocardial infarction (AMI) could cause desquamation of endothelial cells in circulating blood compared with effort angina (EA) and noncoronary chest pain. A high CEC count was found in AMI (median, 7.5 cells/mL; interquartile range, 4.1 to 43.5, P &lt; .01 analysis of variance

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Mutin, Murielle, Isabelle Canavy, Andrew Blann, Michel Bory, José Sampol, and Françoise Dignat-George. "Direct Evidence of Endothelial Injury in Acute Myocardial Infarction and Unstable Angina by Demonstration of Circulating Endothelial Cells." Blood 93, no. 9 (1999): 2951–58. http://dx.doi.org/10.1182/blood.v93.9.2951.409k02_2951_2958.

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Circulating endothelial cells (CECs) have been detected in association with endothelial injury and therefore represent proof of serious damage to the vascular tree. Our aim was to investigate, using the technique of immunomagnetic separation, whether the pathological events in unstable angina (UA) or acute myocardial infarction (AMI) could cause desquamation of endothelial cells in circulating blood compared with effort angina (EA) and noncoronary chest pain. A high CEC count was found in AMI (median, 7.5 cells/mL; interquartile range, 4.1 to 43.5, P < .01 analysis of variance [ANOVA]) and

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Millar, Michelle Warren, Fabeha Fazal та Arshad Rahman. "Therapeutic Targeting of NF-κB in Acute Lung Injury: A Double-Edged Sword". Cells 11, № 20 (2022): 3317. http://dx.doi.org/10.3390/cells11203317.

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Acute lung injury/acute respiratory distress syndrome (ALI/ARDS) is a devastating disease that can be caused by a variety of conditions including pneumonia, sepsis, trauma, and most recently, COVID-19. Although our understanding of the mechanisms of ALI/ARDS pathogenesis and resolution has considerably increased in recent years, the mortality rate remains unacceptably high (~40%), primarily due to the lack of effective therapies for ALI/ARDS. Dysregulated inflammation, as characterized by massive infiltration of polymorphonuclear leukocytes (PMNs) into the airspace and the associated damage of

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Su, Vincent Yi-Fong, Shih-Hwa Chiou, Wei-Chih Chen, et al. "Induced Pluripotent Stem Cell-Derived Conditioned Medium Promotes Endogenous Leukemia Inhibitory Factor to Attenuate Endotoxin-Induced Acute Lung Injury." International Journal of Molecular Sciences 22, no. 11 (2021): 5554. http://dx.doi.org/10.3390/ijms22115554.

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The conditioned medium of induced pluripotent stem cells (iPSC-CM) can attenuate neutrophil recruitment and endothelial leakage of lipopolysaccharide (LPS)-induced acute lung injury (ALI). Therefore, we investigated the mechanisms by which iPSC-CM regulate the interaction between neutrophils and the endothelium in ALI. Murine iPSCs (miPSCs) were delivered intravenously to male C57BL/6 mice (8–12 weeks old) 4 h after intratracheal LPS injection. A miPSC-derived conditioned medium (miPSC-CM) was delivered intravenously to mice after intratracheal LPS injection. DMSO-induced HL-60 cells (D-HL-60,

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MOREY, K. Anjali, Mahnaz RAZANDI, Ali PEDRAM, Ren-Ming HU, A. Bruce PRINS, and R. Ellis LEVIN. "Oestrogen and progesterone inhibit the stimulated production of endothelin-1." Biochemical Journal 330, no. 3 (1998): 1097–105. http://dx.doi.org/10.1042/bj3301097.

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Important vascular proteins such as endothelin-1 (ET-1) promote the development of cardiovascular diseases. Oestrogen, and perhaps progesterone, prevent the development of vascular disease in women through incompletely understood cellular mechanisms. We hypothesized that oestradiol or progesterone might regulate the production of ET-1 as a potential novel mechanism. We found that serum and angiotensin II (AII) significantly stimulated ET-1 secretion from cultured bovine aortic endothelial cells, inhibited 50-75% by oestradiol or by progesterone. Serum and AII stimulated ET-1 mRNA levels, inhib

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Yin, Yujie, Qian Zhang, Qifei Zhao, et al. "Tongxinluo Attenuates Myocardiac Fibrosis after Acute Myocardial Infarction in Rats via Inhibition of Endothelial-to-Mesenchymal Transition." BioMed Research International 2019 (June 16, 2019): 1–13. http://dx.doi.org/10.1155/2019/6595437.

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Endothelial-to-mesenchymal transition (EndMT) is an essential mechanism in myocardial fibrosis (MF). Tongxinluo (TXL) has been confirmed to protect the endothelium against reperfusion injury after acute myocardial infarction (AMI). However, whether TXL can inhibit MF after AMI via inhibiting EndMT remained unknown. This study aims to identify the role of EndMT in MF after AMI as well as the protective effects and underlying mechanisms of TXL on MF. The AMI model was established in rats by ligating left anterior descending coronary artery. Then, rats were administered with high- (0.8 g·kg−1·d−1

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Wu, Yanyan, Rong Huang, Xu Zhong, and Yi Xiao. "Cardiovascular Consequences of Repetitive Arousals over the Entire Sleep Duration." BioMed Research International 2017 (2017): 1–8. http://dx.doi.org/10.1155/2017/4213861.

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Objectives. To explore the cardiovascular effects of nightlong repetitive arousals (RA).Methods. Twenty healthy subjects participated in two consecutive sleep studies. The first one was free of intervention and the second study involved repetitive arousals induced by acoustical stimuli. Blood pressure, heart rate variability (HRV), arterial stiffness index (ASI), and serum markers including nitric oxide (NO), endothelin-1 (ET-1), C-reactive protein (CRP), interleukin-6 (IL-6), tumor necrosis factor-α(TNF-α), and vascular endothelial growth factor (VEGF) were studied.Results. RA led to overnigh

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Wu, Xiaoyan, Rongqing Guo, Peili Chen, Quan Wang, and Patrick N. Cunningham. "TNF induces caspase-dependent inflammation in renal endothelial cells through a Rho- and myosin light chain kinase-dependent mechanism." American Journal of Physiology-Renal Physiology 297, no. 2 (2009): F316—F326. http://dx.doi.org/10.1152/ajprenal.00089.2009.

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The pathogenesis of LPS-induced acute kidney injury (AKI) requires signaling through tumor necrosis factor-α (TNF) receptor 1 (TNFR1), which within the kidney is primarily located in the endothelium. We showed previously that caspase inhibition protected mice against LPS-induced AKI and in parallel significantly inhibited LPS-induced renal inflammation. Therefore we hypothesized that caspase activation amplifies TNF-induced inflammation in renal endothelial cells (ECs). In cultured renal ECs, TNF induced apoptosis through a caspase-8-dependent pathway. TNF caused translocation of the p65 subun

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NYSTRÖM, Thomas, Arne NYGREN, and Åke SJÖHOLM. "Persistent endothelial dysfunction is related to elevated C-reactive protein (CRP) levels in Type II diabetic patients after acute myocardial infarction." Clinical Science 108, no. 2 (2005): 121–28. http://dx.doi.org/10.1042/cs20040243.

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The atherosclerotic process is an ongoing dynamic and progressive state arising from endothelial dysfunction and inflammation. Although suffering from an acute coronary artery disease, patients with Type II diabetes have a poor outcome compared with non-diabetic patients, which may only partly be explained by traditional risk factors. Our purpose was to compare non-traditional risk factors, such as endothelial function, C-reactive protein (CRP) and adiponectin, in Type II diabetic and non-diabetic patients following AMI (acute myocardial infarction). Twenty Type II diabetic patients were compa

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Kwon, Osun, Seok-Min Hong, and Ganesan Ramesh. "Diminished NO generation by injured endothelium and loss of macula densa nNOS may contribute to sustained acute kidney injury after ischemia-reperfusion." American Journal of Physiology-Renal Physiology 296, no. 1 (2009): F25—F33. http://dx.doi.org/10.1152/ajprenal.90531.2008.

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In postischemic acute kidney injury (AKI) or acute renal failure, a dissipation of glomerular filtration pressure is associated with an altered renal vascular tone and reactivity, as well as a loss of vascular autoregulation. To test the hypothesis that renal nitric oxide (NO) generation reflects endothelial damage in the kidney after ischemia-reperfusion, we quantified the urinary NO levels and identified the site of its generation in postischemic AKI. Subjects were 50 recipients of cadaveric renal allografts: 15 with sustained AKI and 35 with recovering renal function. Urine and blood sample

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Schunk, Stefan J., Sarah Triem, David Schmit та ін. "Interleukin-1α Is a Central Regulator of Leukocyte-Endothelial Adhesion in Myocardial Infarction and in Chronic Kidney Disease". Circulation 144, № 11 (2021): 893–908. http://dx.doi.org/10.1161/circulationaha.121.053547.

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Background: Cardiovascular diseases and chronic kidney disease (CKD) are highly prevalent, aggravate each other, and account for substantial mortality. Both conditions are characterized by activation of the innate immune system. The alarmin interleukin-1α (IL-1α) is expressed in a variety of cell types promoting (sterile) systemic inflammation. The aim of the present study was to examine the role of IL-1α in mediating inflammation in the setting of acute myocardial infarction (AMI) and CKD. Methods: We assessed the expression of IL-1α on the surface of monocytes from patients with AMI and pati

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Hassoun, Heitham T., Mihaela L. Lie, Dmitry N. Grigoryev, Manchang Liu, Rubin M. Tuder, and Hamid Rabb. "Kidney ischemia-reperfusion injury induces caspase-dependent pulmonary apoptosis." American Journal of Physiology-Renal Physiology 297, no. 1 (2009): F125—F137. http://dx.doi.org/10.1152/ajprenal.90666.2008.

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Distant organ effects of acute kidney injury (AKI) are a leading cause of morbidity and mortality. While little is known about the underlying mechanisms, limited data suggest a role for inflammation and apoptosis. Utilizing a lung candidate gene discovery approach in a mouse model of ischemic AKI-induced lung dysfunction, we identified prominent lung activation of 66 apoptosis-related genes at 6 and/or 36 h following ischemia, of which 6 genes represent the tumor necrosis factor receptor (TNFR) superfamily, and another 23 genes are associated with the TNFR pathway. Given that pulmonary apoptos

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Yin, Jie, Hong Chang, Dongmei Wang, Haifei Li, and Aibing Yin. "Fuzzy C-Means Clustering Algorithm-Based Magnetic Resonance Imaging Image Segmentation for Analyzing the Effect of Edaravone on the Vascular Endothelial Function in Patients with Acute Cerebral Infarction." Contrast Media & Molecular Imaging 2021 (July 14, 2021): 1–8. http://dx.doi.org/10.1155/2021/4080305.

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This paper aimed to discuss the denoising ability of magnetic resonance imaging (MRI) images based on fuzzy C-means clustering (FCM) algorithm and the influence of Butylphthalide combined with Edaravone treatment on nerve function and vascular endothelial function in patients with acute cerebral infarction (ACI). Based on FCM algorithm, Markov Random Field (MRF) model algorithm was introduced to obtain a novel algorithm (NFCM), which was compared with FCM and MRF algorithm in terms of misclassification rate (MCR) and difference of Kappa index (KI). 90 patients with ACI diagnosed in hospital fr

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Koren-Michowitz, Maya, Batia Avni, Irma Zur, et al. "Endothelial Function in Patients with Essential Thrombocytosis." Blood 106, no. 11 (2005): 3983. http://dx.doi.org/10.1182/blood.v106.11.3983.3983.

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Abstract Essential thrombocytosis (ET) is a myeloproliferative disorder whose main complication is thrombothic events. Reduction of platelet count is associated with a decrease in the risk for thrombosis. Recently it was shown that although anagrelide and hydroxyurea lower platelet counts to the same extent, hydroxyurea decreased the rate of arterial thrombosis and increased the rate of venous thrombosis compared to anagrelide. The reason for the different effects is unknown. The endothelium has important antithrombotic properties. Therefore, we hypothesized that hydroxyurea and anagrelide may

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Viñas, Jose L., Christopher J. Porter, Adrianna Douvris, et al. "Sex diversity in proximal tubule and endothelial gene expression in mice with ischemic acute kidney injury." Clinical Science 134, no. 14 (2020): 1887–909. http://dx.doi.org/10.1042/cs20200168.

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Abstract Female sex protects against development of acute kidney injury (AKI). While sex hormones may be involved in protection, the role of differential gene expression is unknown. We conducted gene profiling in male and female mice with or without kidney ischemia–reperfusion injury (IRI). Mice underwent bilateral renal pedicle clamping (30 min), and tissues were collected 24 h after reperfusion. RNA-sequencing (RNA-Seq) was performed on proximal tubules (PTs) and kidney endothelial cells. Female mice were resistant to ischemic injury compared with males, determined by plasma creatinine and n

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Phillips, Shane A., Kimberly R. Pechman, Ellen C. Leonard, et al. "Increased ANG II sensitivity following recovery from acute kidney injury: role of oxidant stress in skeletal muscle resistance arteries." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 298, no. 6 (2010): R1682—R1691. http://dx.doi.org/10.1152/ajpregu.00448.2009.

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Ischemia-reperfusion (I/R)-induced acute kidney injury (AKI) results in prolonged impairment of peripheral (i.e., nonrenal) vascular function since skeletal muscle resistance arteries derived from rats 5 wk post-I/R injury, show enhanced responses to ANG II stimulation but not other constrictors. Because vascular superoxide increases ANG II sensitivity, we hypothesized that peripheral responsiveness following recovery from AKI was attributable to vascular oxidant stress. Gracilis arteries (GA) isolated from post-I/R rats (∼5 wk recovery) showed significantly greater superoxide levels relative

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Liang, Emily C., Erik L. Kimble, Aya Albittar, et al. "Phase I/II Study to Evaluate the Safety, Feasibility, and Efficacy of FP-1201 (Intravenous Interferon-Beta-1a) to Prevent Toxicities after CD19-Directed CAR T-Cell Therapy: Trial in Progress." Blood 142, Supplement 1 (2023): 4860. http://dx.doi.org/10.1182/blood-2023-173152.

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BACKGROUND CD19 chimeric antigen receptor (CAR) T-cell therapy has revolutionized the treatment of patients with relapsed/refractory B-cell malignancies. Yet it remains limited by potentially life-threatening toxicities such as CRS and ICANS. The risk of CRS and ICANS restricts the use of CD19 CAR T-cell therapy to large academic centers and leads to high healthcare resource utilization. Current toxicity prevention strategies have shown limited efficacy to date (prophylactic steroids with axi-cel: CRS, 80%; ICANS, 60%; Oluwole, BJH, 2021; early intervention with brexu-cel: CRS, 89%; ICANS, 60%

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Wang, Wei, Einath Zolty, Sandor Falk, et al. "Prostacyclin in endotoxemia-induced acute kidney injury: cyclooxygenase inhibition and renal prostacyclin synthase transgenic mice." American Journal of Physiology-Renal Physiology 293, no. 4 (2007): F1131—F1136. http://dx.doi.org/10.1152/ajprenal.00212.2007.

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Sepsis-related acute kidney injury (AKI) is the leading cause of AKI in intensive care units. Endotoxin is a primary initiator of inflammatory and hemodynamic consequences of sepsis and is associated with experimental AKI. The present study was undertaken to further examine the role of the endothelium, specifically prostacyclin (PGI2), in the pathogenesis of endotoxemia-related AKI. A low dose of endotoxin (LPS, 1 mg/kg) in wild-type (WT) mice was associated with stable glomerular filtration rate (GFR) (164.0 ± 16.7 vs. 173.3 ± 6.7 μl/min, P = not significant) as urinary excretion of 6-keto-PG

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Liu, Zhifeng, Jingjing Ji, Dong Zheng, Lei Su, Tianqing Peng, and Jing Tang. "Protective role of endothelial calpain knockout in lipopolysaccharide-induced acute kidney injury via attenuation of the p38-iNOS pathway and NO/ROS production." Experimental & Molecular Medicine 52, no. 4 (2020): 702–12. http://dx.doi.org/10.1038/s12276-020-0426-9.

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Abstract To explore the role of calpain and its signaling pathway in lipopolysaccharide (LPS)-induced acute kidney injury (AKI), animal models of endotoxemia were established by administration of LPS to mice with endothelial-specific Capn4 knockout (TEK/Capn4−/−), mice with calpastatin (an endogenous calpain inhibitor) overexpression (Tg-CAST) and mice with myeloid-specific Capn4 knockout (LYZ/Capn4−/−). Mouse pulmonary microvascular endothelial cells (PMECs) were used as a model of the microvascular endothelium and were stimulated with LPS. Renal function, renal inducible nitric oxide synthas

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MIURA, Y., C. ITOH, T. MIYAKAWA, et al. "SIMULTANEOUS DETERMINATION OF TRACE ELEMENTS IN SERA OF PATIENTS WITH ACUTE MYOCARDIAL INFARCTION BY PIXE -2-." International Journal of PIXE 05, no. 01 (1995): 33–38. http://dx.doi.org/10.1142/s012908359500006x.

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Vascular cell adhesion molecule-1 (VCAM-1) is transiently expressed on vascular endothelial cells in response to cytokines. It plays a major role in the adhesion of leucocytes to the endothelium by interaction with its ligand VLA-4, a member of the β1 integrin family. We measured the serum concentration of the soluble VCAM-1 (sVCAM-1) in 114 patients with acute myocardial infarction (AMI) and 37 normal controls by enzyme-linked immunoassay in comparison with trace element concentration. sVCAM-1 levels were markedly higher (mean± SD=833.2±328.9 ng/ml) in the sera of patients with AMI than in no

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MIURA, Y., C. ITOH, T. MIYAKAWA, et al. "SIMULTANEOUS DETERMINA TION OF TRACE ELEMENTS IN SERA OF PATIENTS WITH ACUTE MYOCARDIAL INFARCTION BY PIXE -2-." International Journal of PIXE 06, no. 01n02 (1996): 233–40. http://dx.doi.org/10.1142/s0129083596000235.

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Vascular cell adhesion molecule-1 (VCAM-1) is transiently expressed on vascular endothelial cells in response to cytokines. It plays a major role in the adhesion of leucocytes to the endothelium by interaction with its ligand VLA-4, a member of the β1 integrin family. We measured the serum concentration of the soluble VCAM-1 (sVCAM-1) in 114 patients with acute myocardial infarction (AMI) and 37 normal controls by enzyme-linked immunoassay in comparison with trace element concentration. sVCAM-1 levels were markedly higher ( mean ± SD =833.2 ± 328.9 ng/ml ) in the sera of patients with AMI than

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Wang, Wei, Einath Zolty, Sandor Falk, et al. "Endotoxemia-related acute kidney injury in transgenic mice with endothelial overexpression of GTP cyclohydrolase-1." American Journal of Physiology-Renal Physiology 294, no. 3 (2008): F571—F576. http://dx.doi.org/10.1152/ajprenal.00538.2007.

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Endotoxin-related acute kidney injury has been shown to profoundly induce nitric oxide (NO), which activates sympathetic and renin-angiotensin system, resulting in renal vasoconstriction. While vascular muscle cells are known to upregulate inducible NO synthase (iNOS), less is known about the endothelium as a source of NO during endotoxemia. Studies were, therefore, undertaken both in vitro in mouse microvascular endothelial cells and in vivo in transgenic mice with overexpression of endothelial GTP cyclohydrolase, the rate-limiting enzyme for tetrahydrobiopterin, a cofactor for NO synthase. L

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Zhuo, Wei, Xiaomin Song, Hao Zhou, and Yongzhang Luo. "Arginine deiminase modulates endothelial tip cells via excessive synthesis of reactive oxygen species." Biochemical Society Transactions 39, no. 5 (2011): 1376–81. http://dx.doi.org/10.1042/bst0391376.

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ADI (arginine deiminase), an enzyme that hydrolyses arginine, has been reported as an anti-angiogenesis agent. However, its molecular mechanism is unclear. We have demonstrated for the first time that ADI modulates the angiogenic activity of endothelial tip cells. By arginine depletion, ADI disturbs actin filament in endothelial tip cells, causing disordered migratory direction and decreased migration ability. Furthermore, ADI induces excessive synthesis of ROS (reactive oxygen species), and activates caspase 8-, but not caspase 9-, dependent apoptosis in endothelial cells. These findings prov

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