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Artykuły w czasopismach na temat „Kidney inflammation”

Autor: Grafiati

Data publikacji: 2 czerwca 2025

Data aktualizacji: 31 lipca 2025

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1

Tian, Zhi-Kai, Yu-Jia Zhang, Zhao-Jun Feng, et al. "Nephroprotective effect of gastrodin against lead-induced oxidative stress and inflammation in mice by the GSH, Trx, Nrf2 antioxidant system, and the HMGB1 pathway." Toxicology Research 10, no. 2 (2021): 249–63. http://dx.doi.org/10.1093/toxres/tfab003.

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Abstract Gastrodin (GAS), the main phenolic glycoside derivative from Gastrodiaelata Blume, has several bio-activities. However, the molecular mechanisms of these protective actions currently remain unclear. This study aimed to investigate the mechanisms of GAS on lead (Pb)-induced oxidative stress and inflammation in the kidneys and primary kidney mesangial cells. Results indicated that GAS improved Pb-induced renal dysfunction and morphological changes in mice. GAS ameliorated Pb-induced inflammation in kidneys by reducing the TNF-α and IL-6 levels. GAS inhibited Pb-induced oxidative stress

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Jung, Su Woong, Su-Mi Kim, Yang Gyun Kim, Sang-Ho Lee, and Ju-Young Moon. "Uric acid and inflammation in kidney disease." American Journal of Physiology-Renal Physiology 318, no. 6 (2020): F1327—F1340. http://dx.doi.org/10.1152/ajprenal.00272.2019.

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Asymptomatic hyperuricemia is frequently observed in patients with kidney disease. Although a substantial number of epidemiologic studies have suggested that an elevated uric acid level plays a causative role in the development and progression of kidney disease, whether hyperuricemia is simply a result of decreased renal excretion of uric acid or is a contributor to kidney disease remains a matter of debate. Over the last two decades, multiple experimental studies have expanded the knowledge of the biological effects of uric acid beyond its role in gout. In particular, uric acid induces immune

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Kimura, Tomonori, Yoshitaka Isaka, and Tamotsu Yoshimori. "Autophagy and kidney inflammation." Autophagy 13, no. 6 (2017): 997–1003. http://dx.doi.org/10.1080/15548627.2017.1309485.

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Bachurin, G. V., A. V. Bachurin, and Yu S. Kolomoets. "Enzyme test – early diagnosis of kidney inflammation." Urologiya 28, no. 1-4 (2024): 38–48. https://doi.org/10.26641/2307-5279.28.1-4.2024.322090.

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The aim of the work is to improve the results of early diagnosis of acute infectious kidney diseases at the molecular level in urolithiasis (urinary stone disease) through the study of enzymatic test indicators. Enzymatic tests (NGAL, IL-1β, β2-microglobulin) were investigated at the molecular level using the IFA method in the urine of patients with urolithiasis. Comparative and prognostic significance of the conducted treatment was established between the groups of patients, and an algorithm was developed based on the results of kidney damage predictors. It was found that the indicators of ge

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Goesch, Torsten R., Nancy A. Wilson, Weifeng Zeng, et al. "Suppression of Inflammation-Associated Kidney Damage Post-Transplant Using the New PrC-210 Free Radical Scavenger in Rats." Biomolecules 11, no. 7 (2021): 1054. http://dx.doi.org/10.3390/biom11071054.

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Allograft kidney transplantation, which triggers host cellular- and antibody-mediated rejection of the kidney, is a major contributor to kidney damage during transplant. Here, we asked whether PrC-210 would suppress damage seen in allograft kidney transplant. Brown Norway (BN) rat kidneys were perfused in situ (UW Solution) with or without added 30 mM PrC-210, and then immediately transplanted into Lewis (LEW) rats. 20 h later, the transplanted BN kidneys and LEW rat plasma were analyzed. Kidney histology, and kidney/serum levels of several inflammation-associated cytokines, were measured to a

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Akcay, Ali, Quocan Nguyen, and Charles L. Edelstein. "Mediators of Inflammation in Acute Kidney Injury." Mediators of Inflammation 2009 (2009): 1–12. http://dx.doi.org/10.1155/2009/137072.

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Acute kidney injury (AKI) remains to be an independent risk factor for mortality and morbidity. Inflammation is now believed to play a major role in the pathopathophysiology of AKI. It is hypothesized that in ischemia, sepsis and nephrotoxic models that the initial insult results in morphological and/or functional changes in vascular endothelial cells and/or in tubular epithelium. Then, leukocytes including neutrophils, macrophages, natural killer cells, and lymphocytes infiltrate into the injured kidneys. The injury induces the generation of inflammatory mediators like cytokines and chemokine

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Perry, Heather M., Nicole Görldt, Sun-sang J. Sung, et al. "Perivascular CD73+ cells attenuate inflammation and interstitial fibrosis in the kidney microenvironment." American Journal of Physiology-Renal Physiology 317, no. 3 (2019): F658—F669. http://dx.doi.org/10.1152/ajprenal.00243.2019.

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Progressive tubulointerstitial fibrosis may occur after acute kidney injury due to persistent inflammation. Purinergic signaling by 5′-ectonucleotidase, CD73, an enzyme that converts AMP to adenosine on the extracellular surface, can suppress inflammation. The role of CD73 in progressive kidney fibrosis has not been elucidated. We evaluated the effect of deletion of CD73 from kidney perivascular cells (including pericytes and/or fibroblasts of the Foxd1+ lineage) on fibrosis. Perivascular cell expression of CD73 was necessary to suppress inflammation and prevent kidney fibrosis in Foxd1CreCD73

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Huang, Liang-Ti, and Chung-Ming Chen. "Kidney Injuries and Evolution of Chronic Kidney Diseases Due to Neonatal Hyperoxia Exposure Based on Animal Studies." International Journal of Molecular Sciences 23, no. 15 (2022): 8492. http://dx.doi.org/10.3390/ijms23158492.

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Preterm birth interrupts the development and maturation of the kidneys during the critical growth period. The kidneys can also exhibit structural defects and functional impairment due to hyperoxia, as demonstrated by various animal studies. Furthermore, hyperoxia during nephrogenesis impairs renal tubular development and induces glomerular and tubular injuries, which manifest as renal corpuscle enlargement, renal tubular necrosis, interstitial inflammation, and kidney fibrosis. Preterm birth along with hyperoxia exposure induces a pathological predisposition to chronic kidney disease. Hyperoxi

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Baer, Brandon, Jason Lin, Kaitlyn R. Schaaf, Lorraine B. Ware, Ciara M. Shaver, and Julie A. Bastarache. "Matrix metalloproteinase-7 is dispensable in a mouse model of sepsis-induced acute lung injury." PLOS One 20, no. 5 (2025): e0321349. https://doi.org/10.1371/journal.pone.0321349.

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Acute respiratory distress syndrome (ARDS) is a life-threatening form of acute lung injury whose pathogenesis is characterized by excessive lung inflammation and alveolar-capillary barrier permeability. Matrix metalloproteinase 7 (MMP7) can regulate leukocyte recruitment and the production of pro-inflammatory cytokines, but whether it plays a role in acute lung injury (ALI) is an unanswered question. We hypothesized that global loss of MMP7 would attenuate sepsis-induced ALI and systemic inflammation. To test this, male and female MMP7 knockout (MMP7KO) mice and wild-type (WT) littermates were

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García-García, Patricia M. "Inflammation in diabetic kidney disease." World Journal of Diabetes 5, no. 4 (2014): 431. http://dx.doi.org/10.4239/wjd.v5.i4.431.

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Krane, Vera, and Christoph Wanner. "Statins, inflammation and kidney disease." Nature Reviews Nephrology 7, no. 7 (2011): 385–97. http://dx.doi.org/10.1038/nrneph.2011.62.

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Pérez-Morales, Rosa E., María Dolores del Pino, José Manuel Valdivielso, Alberto Ortiz, Carmen Mora-Fernández, and Juan F. Navarro-González. "Inflammation in Diabetic Kidney Disease." Nephron 143, no. 1 (2018): 12–16. http://dx.doi.org/10.1159/000493278.

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Mei, Changlin, and Feng Zheng. "Chronic Inflammation Potentiates Kidney Aging." Seminars in Nephrology 29, no. 6 (2009): 555–68. http://dx.doi.org/10.1016/j.semnephrol.2009.07.002.

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Baer, Koch, and Geiger. "Kidney Inflammation, Injury and Regeneration." International Journal of Molecular Sciences 21, no. 3 (2020): 1164. http://dx.doi.org/10.3390/ijms21031164.

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Kinsey, Gilbert R., Li Li, and Mark D. Okusa. "Inflammation in Acute Kidney Injury." Nephron Experimental Nephrology 109, no. 4 (2008): e102-e107. http://dx.doi.org/10.1159/000142934.

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Navarro-Díaz, Maruja, Assumpta Serra, Dolores López, Marisa Granada, Beatriz Bayés, and Ramón Romero. "Obesity, inflammation, and kidney disease." Kidney International 74 (December 2008): S15—S18. http://dx.doi.org/10.1038/ki.2008.518.

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Jang, Kyu Won, Jin Hur, Dong Won Lee, and Seo Rin Kim. "Metabolic Syndrome, Kidney-Related Adiposity, and Kidney Microcirculation: Unraveling the Damage." Biomedicines 12, no. 12 (2024): 2706. http://dx.doi.org/10.3390/biomedicines12122706.

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Metabolic syndrome (MetS) is a cluster of interrelated risk factors, including insulin resistance, hypertension, dyslipidemia, and visceral adiposity, all of which contribute to kidney microvascular injury and the progression of chronic kidney disease (CKD). However, the specific impact of each component of MetS on kidney microcirculation remains unclear. Given the increasing prevalence of obesity, understanding how visceral fat—particularly fat surrounding the kidneys—affects kidney microcirculation is critical. This review examines the consequences of visceral obesity and other components of

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Gusev, Evgenii, Liliya Solomatina, Yulia Zhuravleva, and Alexey Sarapultsev. "The Pathogenesis of End-Stage Renal Disease from the Standpoint of the Theory of General Pathological Processes of Inflammation." International Journal of Molecular Sciences 22, no. 21 (2021): 11453. http://dx.doi.org/10.3390/ijms222111453.

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Chronic kidney disease can progress to end-stage chronic renal disease (ESRD), which requires the use of replacement therapy (dialysis or kidney transplant) in life-threatening conditions. In ESRD, irreversible changes in the kidneys are associated with systemic changes of proinflammatory nature and dysfunctions of internal organs, skeletal muscles, and integumentary tissues. The common components of ESRD pathogenesis, regardless of the initial nosology, are (1) local (in the kidneys) and systemic chronic low-grade inflammation (ChLGI) as a risk factor for diabetic kidney disease and its progr

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Black, L. M., J. M. Lever, A. M. Traylor, et al. "Divergent effects of AKI to CKD models on inflammation and fibrosis." American Journal of Physiology-Renal Physiology 315, no. 4 (2018): F1107—F1118. http://dx.doi.org/10.1152/ajprenal.00179.2018.

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Chronic kidney disease (CKD) is a condition with significant morbidity and mortality that affects 15% of adults in the United States. One cause of CKD is acute kidney injury (AKI), which commonly occurs secondary to sepsis, ischemic events, and drug-induced nephrotoxicity. Unilateral ischemia-reperfusion injury (UIRI) without contralateral nephrectomy (CLN) and repeated low-dose cisplatin (RLDC) models of AKI to CKD demonstrate responses characteristic of the transition; however, previous studies have not effectively compared the pathogenesis. We demonstrate both models instigate renal dysfunc

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Teshaev Shukhrat Zhumaevich, Khamdamova Mukhayokhon Tukhtasinovna, and Khikmatova Madina Furkatovna. "Protective effect of pomegranate seed oil against salt toxicity in rat kidneys." Texas Journal of Medical Science 27 (December 12, 2023): 57–59. http://dx.doi.org/10.62480/tjms.2023.vol27.pp57-59.

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Consuming too much salt can have a negative impact on your kidneys. The kidneys play an important role in regulating sodium levels in the body, and excess salt can lead to water retention and increased blood pressure, which in turn can have a negative impact on the kidneys. Excess salt in the diet can contribute to the formation of kidney stones. This is because excess sodium can lead to increased calcium excretion in the urine, which in turn increases the risk of stone formation. An experiment was conducted on rats to study the effect of salt on kidney function. During the experiment, a group

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Byers, Aaron, Nicholas Herrera, and Itunu Owoyemi. "Chronic inflammation and calciphylaxis." BMJ Case Reports 15, no. 4 (2022): e248668. http://dx.doi.org/10.1136/bcr-2021-248668.

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Calciphylaxis also known as calcific uraemic arteriolopathy is a rare condition mostly seen in patients with end-stage kidney disease. We report a case of a simultaneous-kidney-pancreas transplant patient with functioning grafts developing biopsy-proven calciphylaxis in the setting of chronic inflammation. Despite several modalities of management, the patient developed progression of her disease leading to multiple amputations. This case illustrates chronic inflammation driven by persistent infection as a probable contributing factor to the development and progression of calciphylaxis in a sim

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Martin-Sanchez, Diego, Juan Guerrero-Mauvecin, Miguel Fontecha-Barriuso, et al. "Bone Marrow–Derived RIPK3 Mediates Kidney Inflammation in Acute Kidney Injury." Journal of the American Society of Nephrology 33, no. 2 (2022): 357–73. http://dx.doi.org/10.1681/asn.2021030383.

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BackgroundReceptor-interacting protein kinase 3 (RIPK3), a component of necroptosis pathways, may have an independent role in inflammation. It has been unclear which RIPK3-expressing cells are responsible for the anti-inflammatory effect of overall Ripk3 deficiency and whether Ripk3 deficiency protects against kidney inflammation occurring in the absence of tubular cell death.MethodsWe used chimeric mice with bone marrow from wild-type and Ripk3-knockout mice to explore RIPK3′s contribution to kidney inflammation in the presence of folic acid–induced acute kidney injury AKI (FA-AKI) or absence

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Sun, Ying, Yue Zhang, Daqiang Zhao, et al. "Rotenone Remarkably Attenuates Oxidative Stress, Inflammation, and Fibrosis in Chronic Obstructive Uropathy." Mediators of Inflammation 2014 (2014): 1–9. http://dx.doi.org/10.1155/2014/670106.

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Mitochondrial abnormality has been shown in many kidney disease models. However, its role in the pathogenesis of chronic kidney diseases (CKDs) is still uncertain. In present study, a mitochondrial complex I inhibitor rotenone was applied to the mice subjected to unilateral ureteral obstruction (UUO). Following 7-days rotenone treatment, a remarkable attenuation of tubular injury was detected by PAS staining. In line with the improvement of kidney morphology, rotenone remarkably blunted fibrotic response as shown by downregulation of fibronectin (FN), plasminogen activator inhibitor-1 (PAI-1),

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Wang, Bo, Chenguang Ding, Xiaoming Ding та ін. "WNT1-inducible signaling pathway protein 1 regulates kidney inflammation through the NF-κB pathway". Clinical Science 136, № 1 (2022): 29–44. http://dx.doi.org/10.1042/cs20210663.

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Abstract Inflammation is a pathological feature of kidney injury and its progression correlates with the development of kidney fibrosis which can lead to kidney function impairment. This project investigated the regulatory function of WNT1-inducible signaling pathway protein 1 (WISP1) in kidney inflammation. Administration of recombinant WISP1 protein to healthy mice induced kidney inflammation (macrophage accrual and production of tumor necrosis factor α (TNF-α), CCL2 and IL-6), which could be prevented by inhibition of nuclear factor κ-light-chain-enhancer of activated B cells (NF-κB). Furth

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Alamsyah, Firman, Nisrina Firdausi, Subekti Evi Dwi Nugraheni, et al. "Effects of non-contact electric fields on kidney and liver histology in tumour-induced rats." F1000Research 12 (November 22, 2024): 117. http://dx.doi.org/10.12688/f1000research.110080.5.

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Background A novel modality of cancer treatment based on exposure to non-contact electric fields has been developed to reduce cancer incidence. However, the safety of the electric field exposure was not fully investigated. Therefore, This study aimed to observe the safety of electric field exposure on kidney and liver structures. Methods Female Sprague-Dawley rats were divided into one control group and three treatment groups. Animals were treated with 7,12-dimethylbenz[a]anthracene for mammary tumour induction and exposed to non-contact electric fields individually for 10 hours a day for thre

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Alamsyah, Firman, Nisrina Firdausi, Subekti Evi Dwi Nugraheni, et al. "Effects of non-contact electric fields on kidney and liver histology in tumour-induced rats." F1000Research 12 (January 8, 2024): 117. http://dx.doi.org/10.12688/f1000research.110080.4.

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Background A novel modality of cancer treatment based on exposure to non-contact electric fields has been developed to reduce cancer incidence. However, the safety of the electric field exposure was not fully investigated. Therefore, This study aimed to observe the safety of electric field exposure on kidney and liver structures. Methods Female Sprague-Dawley rats were divided into one control group and three treatment groups. Animals were treated with 7,12-dimethylbenz[a]anthracene for mammary tumour induction and exposed to non-contact electric fields individually for 10 hours a day for thre

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Anandh, Urmila, and Anita Saxena. "Controlling Oxidative Stress and Inflammation in Chronic Kidney Disease: The Role of Nutritional Interventions." Journal of Renal Nutrition and Metabolism 9, no. 1 (2024): 2–9. http://dx.doi.org/10.4103/jrnm.jrnm_1_23.

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Multiple factors impact the kidney health. Underlying comorbidities (diabetes and hypertension), medications, genetic predisposition, autoimmunity, and environmental insults play an important role. The vulnerability of the kidneys is to some extent because of the large proportion of blood it receives. It is the recipient of multiple deleterious substances with very little defense mechanisms. Over the years, low-grade subclinical inflammation and oxidative stress have been shown to play an important role in the progression of chronic kidney disease (CKD). Kidneys unfortunately have very little

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Anandh, Urmila, and Anita Saxena. "Controlling Oxidative Stress and Inflammation in Chronic Kidney Disease: The Role of Nutritional Interventions." Journal of Renal Nutrition and Metabolism 8, no. 1 (2023): 16–23. http://dx.doi.org/10.4103/jrnm.jrnm_6_23.

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Multiple factors impact kidney health. Underlying comorbidities (diabetes and hypertension), medications, genetic predisposition, autoimmunity, and environmental insults all play an important role. The vulnerability of the kidneys is to some extent because of the large proportion of blood it receives. It is the recipient of multiple deleterious substances with very few defense mechanisms. Over the years, low-grade subclinical inflammation and oxidative stress have been shown to play an important role in the progression of chronic kidney disease (CKD). Kidneys unfortunately have very few anti-o

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Du, Chunyang, Tao Zhang, Xia Xiao, Yonghong Shi, Huijun Duan, and Yunzhuo Ren. "Protease-activated receptor-2 promotes kidney tubular epithelial inflammation by inhibiting autophagy via the PI3K/Akt/mTOR signalling pathway." Biochemical Journal 474, no. 16 (2017): 2733–47. http://dx.doi.org/10.1042/bcj20170272.

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Protease-activated receptor-2 (PAR2), which belongs to a specific class of the G-protein-coupled receptors, is central to several inflammation processes. However, the precise molecular mechanism involved remains undefined. Autophagy has been previously shown to affect inflammation. In the present study, we examine the effect of PAR2 on kidney tubular epithelial autophagy and on autophagy-related inflammation and reveal the underlying mechanism involved. Autophagic activity and levels of autophagic marker LC3 were examined in human kidney tubular epithelial cells with PAR2 knockdown or overexpr

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Cao, Qi, David C. H. Harris, and Yiping Wang. "Macrophages in Kidney Injury, Inflammation, and Fibrosis." Physiology 30, no. 3 (2015): 183–94. http://dx.doi.org/10.1152/physiol.00046.2014.

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Macrophages are found in normal kidney and in increased numbers in diseased kidney, where they act as key players in renal injury, inflammation, and fibrosis. Macrophages are highly heterogeneous cells and exhibit distinct phenotypic and functional characteristics in response to various stimuli in the local microenvironment in different types of kidney disease. In kidney tissue necrosis and/or infection, damage- and/or pathogen-associated molecular patterns induce pro-inflammatory macrophages, which contribute to further tissue injury, inflammation, and subsequent fibrosis. Apoptotic cells and

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Lavoz, Carolina, Jonay Poveda, Laura Marquez-Exposito, et al. "Gremlin activates the Notch pathway linked to renal inflammation." Clinical Science 132, no. 11 (2018): 1097–115. http://dx.doi.org/10.1042/cs20171553.

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Preclinical studies suggest that Gremlin participates in renal damage and could be a potential therapeutic target for human chronic kidney diseases. Inflammation is a common characteristic of progressive renal disease, and therefore novel anti-inflammatory therapeutic targets should be investigated. The Notch signaling pathway is involved in kidney development and is activated in human chronic kidney disease, but whether Gremlin regulates the Notch pathway has not been investigated. In cultured tubular cells, Gremlin up-regulated gene expression of several Notch pathway components, increased t

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Rico-Fontalvo, Jorge. "Inflammation and Diabetic Kidney Disease: New Perspectives." J Biomed Res Environ Sci 3, no. 7 (2022): 779–86. https://doi.org/10.37871/jbres1513.

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Diabetic Kidney Disease (DKD) can occur in approximately 30-40% of the population with type 1 or 2 diabetes mellitus around the world. In the pathogenesis and progression the Diabetic Kidney Disease (DKD), three fundamental axes are distinguished: hemodynamic, metabolic and inflammatory. The primary purpose of the review is to describe the role and mechanisms related to inflammation in the course of this disease. The pathophysiological mechanisms involved in the development and progression of DKD include different pathways present long before the clinical diagnosis of the disease. Inflammation

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Wang, Meihui, Zixu Wang, Yaoxing Chen, and Yulan Dong. "Kidney Damage Caused by Obesity and Its Feasible Treatment Drugs." International Journal of Molecular Sciences 23, no. 2 (2022): 747. http://dx.doi.org/10.3390/ijms23020747.

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The rapid growth of obesity worldwide has made it a major health problem, while the dramatic increase in the prevalence of obesity has had a significant impact on the magnitude of chronic kidney disease (CKD), especially in developing countries. A vast amount of researchers have reported a strong relationship between obesity and chronic kidney disease, and obesity can serve as an independent risk factor for kidney disease. The histological changes of kidneys in obesity-induced renal injury include glomerular or tubular hypertrophy, focal segmental glomerulosclerosis or bulbous sclerosis. Furth

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Wanchai, Keerati, Sakawdaurn Yasom, Wannipa Tunapong, et al. "Probiotic Lactobacillus paracasei HII01 protects rats against obese-insulin resistance-induced kidney injury and impaired renal organic anion transporter 3 function." Clinical Science 132, no. 14 (2018): 1545–63. http://dx.doi.org/10.1042/cs20180148.

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The relationship between gut dysbiosis and obesity is currently acknowledged to be a health topic which causes low-grade systemic inflammation and insulin resistance and may damage the kidney. Organic anion transporter 3 (Oat3) has been shown as a transporter responsible for renal handling of gut microbiota products which are involved in the progression of metabolic disorder. The present study investigated the effect of probiotic supplementation on kidney function, renal Oat3 function, inflammation, endoplasmic reticulum (ER) stress, and apoptosis in obese, insulin-resistant rats. After 12 wee

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Kim, Hyun Ju, and Nosratola D. Vaziri. "Contribution of impaired Nrf2-Keap1 pathway to oxidative stress and inflammation in chronic renal failure." American Journal of Physiology-Renal Physiology 298, no. 3 (2010): F662—F671. http://dx.doi.org/10.1152/ajprenal.00421.2009.

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Oxidative stress and inflammation are constant features and major mediators of progression of chronic kidney disease (CKD). Nuclear factor erythroid-2-related factor-2 (Nrf2) confers protection against tissue injury by orchestrating antioxidant and detoxification responses to oxidative and electrophilic stress. While sources of oxidative stress and inflammation in the remnant kidney have been extensively characterized, the effect of CKD on Nrf2 activation and expression of its downstream gene products is unknown and was investigated. Subgroups of male Sprague-Dawley rats were subjected to 5/6

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Pei, Guangchang, Ying Yao, Qian Yang, et al. "Lymphangiogenesis in kidney and lymph node mediates renal inflammation and fibrosis." Science Advances 5, no. 6 (2019): eaaw5075. http://dx.doi.org/10.1126/sciadv.aaw5075.

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Lymphangiogenesis is associated with chronic kidney disease (CKD) and occurs following kidney transplant. Here, we demonstrate that expanding lymphatic vessels (LVs) in kidneys and corresponding renal draining lymph nodes (RDLNs) play critical roles in promoting intrarenal inflammation and fibrosis following renal injury. Our studies show that lymphangiogenesis in the kidney and RDLN is driven by proliferation of preexisting lymphatic endothelium expressing the essential C-C chemokine ligand 21 (CCL21). New injury-induced LVs also express CCL21, stimulating recruitment of more CCR7+dendritic c

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Fan, Heng, Jian-wei Le, Min Sun, and Jian-hua Zhu. "Pretreatment with S-Nitrosoglutathione Attenuates Septic Acute Kidney Injury in Rats by Inhibiting Inflammation, Oxidation, and Apoptosis." BioMed Research International 2021 (February 1, 2021): 1–8. http://dx.doi.org/10.1155/2021/6678165.

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Objective. We aimed to investigate the protective effect of s-nitrosoglutathione (SNG) pretreatment on acute kidney injury (AKI) in septic rats. Methods. We constructed a rat model of sepsis by cecal ligation and puncture and observed the survival of the rats. We obtained kidney and blood samples from rats, observed the pathological damage to the kidney tissues, and evaluated kidney function and the expression levels of inflammatory factors. We also detected the expression of induced nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) in the kidneys by immunohistochemistry and evaluated

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Xu, Zhen E., Yaxi Chen, Ailong Huang, et al. "Inflammatory stress exacerbates lipid-mediated renal injury in ApoE/CD36/SRA triple knockout mice." American Journal of Physiology-Renal Physiology 301, no. 4 (2011): F713—F722. http://dx.doi.org/10.1152/ajprenal.00341.2010.

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Both lipids and inflammation play important roles in the progression of kidney disease. This study was designed to investigate whether inflammation exacerbates lipid accumulation via LDL receptors (LDLr), thereby causing renal injury in C57BL/6J mice, apolipoprotein E (ApoE) knockout (KO) mice, and ApoE/CD36/scavenger receptor A triple KO mice. The mice were given a subcutaneous casein injection to induce inflammatory stress. After 14 wk, terminal blood samples were taken for renal function, lipid profiles, amyloid A (SAA), and IL-6 assays. Lipid accumulation in kidneys was visualized by oil r

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Wang, Tianqi, Xianjun Fu, Qingfa Chen, et al. "Arachidonic Acid Metabolism and Kidney Inflammation." International Journal of Molecular Sciences 20, no. 15 (2019): 3683. http://dx.doi.org/10.3390/ijms20153683.

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As a major component of cell membrane lipids, Arachidonic acid (AA), being a major component of the cell membrane lipid content, is mainly metabolized by three kinds of enzymes: cyclooxygenase (COX), lipoxygenase (LOX), and cytochrome P450 (CYP450) enzymes. Based on these three metabolic pathways, AA could be converted into various metabolites that trigger different inflammatory responses. In the kidney, prostaglandins (PG), thromboxane (Tx), leukotrienes (LTs) and hydroxyeicosatetraenoic acids (HETEs) are the major metabolites generated from AA. An increased level of prostaglandins (PGs), TxA

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Pushpakumar, Sathnur, Subir Kumar Juin, Hebah Almarshood, Dibson Dibe Gondim, Rosemary Ouseph, and Utpal Sen. "Diallyl Trisulfide Attenuates Ischemia-Reperfusion-Induced ER Stress and Kidney Dysfunction in Aged Female Mice." Cells 14, no. 6 (2025): 420. https://doi.org/10.3390/cells14060420.

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Ischemia-reperfusion injury (IRI) is a common cause of acute kidney injury (AKI) in the aging population. Gender studies show that aging is associated with loss of protection from AKI in the female population. While ER stress contributes to IRI-induced AKI in the young, ER regulation during IR in the aged kidney is unclear. Because current evidence suggests hydrogen sulfide (H2S) modulates ER stress, we investigated whether exogenous supplementation of diallyl trisulfide (DATS), an H2S donor, mitigates AKI in aged female kidneys. Wild-type (WT, C57BL/6J) mice aged 75–78 weeks were treated with

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Jo, Min-Jee, Joo-Kyung Lee, Ji-Eun Kim, and Gang-Jee Ko. "Molecular Mechanisms Associated with Aging Kidneys and Future Perspectives." International Journal of Molecular Sciences 24, no. 23 (2023): 16912. http://dx.doi.org/10.3390/ijms242316912.

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The rapid growth of the elderly population is making the need for extensive and advanced information about age-related organ dysfunction a crucial research area. The kidney is one of the organs most affected by aging. Aged kidneys undergo functional decline, characterized by a reduction in kidney size, decreased glomerular filtration rate, alterations in renal blood flow, and increased inflammation and fibrosis. This review offers a foundation for understanding the functional and molecular mechanisms of aging kidneys and for selecting identifying appropriate targets for future treatments of ag

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Stasi, Elodie, Savino Sciascia, Carla Naretto, Simone Baldovino, and Dario Roccatello. "Lymphatic System and the Kidney: From Lymphangiogenesis to Renal Inflammation and Fibrosis Development." International Journal of Molecular Sciences 25, no. 5 (2024): 2853. http://dx.doi.org/10.3390/ijms25052853.

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The lymphatic kidney system plays a crucial role in managing interstitial fluid removal, regulating fluid balance, and tuning immune response. It also assists in the reabsorption of proteins, electrolytes, cytokines, growth factors, and immune cells. Pathological conditions, including tissue damage, excessive interstitial fluid, high blood glucose levels, and inflammation, can initiate lymphangiogenesis—the formation of new lymphatic vessels. This process is associated with various kidney diseases, including polycystic kidney disease, hypertension, ultrafiltration challenges, and complications

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Afarideh, Mohsen, Xin Zhang, Christopher M. Ferguson, et al. "Peristenotic Collateral Circulation in Atherosclerotic Renovascular Disease." Hypertension 76, no. 2 (2020): 497–505. http://dx.doi.org/10.1161/hypertensionaha.120.15057.

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The significance of peristenotic collateral circulation (PCC) development around a stenotic renal artery is unknown. We tested the hypothesis that PCC is linked to loss of kidney function and recovery potential in patients with atherosclerotic renovascular disease (ARVD). Thirty-four patients with ARVD were assigned to medical-therapy with or without revascularization based on clinical indications. The PCC was visualized using multidetector computed tomography and defined relative to segmental arteries in patients with essential hypertension. PCC number before and 3 months after treatment was

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Viau, Amandine, Maroua Baaziz, Amandine Aka, et al. "Tubular STAT3 Limits Renal Inflammation in Autosomal Dominant Polycystic Kidney Disease." Journal of the American Society of Nephrology 31, no. 5 (2020): 1035–49. http://dx.doi.org/10.1681/asn.2019090959.

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BackgroundThe inactivation of the ciliary proteins polycystin 1 or polycystin 2 leads to autosomal dominant polycystic kidney disease (ADPKD). Although signaling by primary cilia and interstitial inflammation both play a critical role in the disease, the reciprocal interactions between immune and tubular cells are not well characterized. The transcription factor STAT3, a component of the cilia proteome that is involved in crosstalk between immune and nonimmune cells in various tissues, has been suggested as a factor fueling ADPKD progression.MethodTo explore how STAT3 intersects with cilia sig

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Huang, Stephanie U.-Shane, Oneli Kulatunge, and Kim Maree O’Sullivan. "Deciphering the Genetic Code of Autoimmune Kidney Diseases." Genes 14, no. 5 (2023): 1028. http://dx.doi.org/10.3390/genes14051028.

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Autoimmune kidney diseases occur due to the loss of tolerance to self-antigens, resulting in inflammation and pathological damage to the kidneys. This review focuses on the known genetic associations of the major autoimmune kidney diseases that result in the development of glomerulonephritis: lupus nephritis (LN), anti-neutrophil cytoplasmic associated vasculitis (AAV), anti-glomerular basement disease (also known as Goodpasture’s disease), IgA nephropathy (IgAN), and membranous nephritis (MN). Genetic associations with an increased risk of disease are not only associated with polymorphisms in

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Baer, Patrick C., Benjamin Koch, and Helmut Geiger. "Kidney Inflammation, Injury and Regeneration 2020." International Journal of Molecular Sciences 22, no. 11 (2021): 5589. http://dx.doi.org/10.3390/ijms22115589.

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Ikizler, T. Alp. "Nutrition, inflammation and chronic kidney disease." Current Opinion in Nephrology and Hypertension 17, no. 2 (2008): 162–67. http://dx.doi.org/10.1097/mnh.0b013e3282f5dbce.

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Inoue, Tsuyoshi, Diane L. Rosin, and Mark D. Okusa. "CAPing inflammation and acute kidney injury." Kidney International 90, no. 3 (2016): 462–65. http://dx.doi.org/10.1016/j.kint.2016.07.009.

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Meissner, Mirjam, Susanne F. Viehmann, and Christian Kurts. "DAMPening sterile inflammation of the kidney." Kidney International 95, no. 3 (2019): 489–91. http://dx.doi.org/10.1016/j.kint.2018.12.007.

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Lee, Chi Ho. "Obesity, inflammation and diabetic kidney disease." Diabetes Research and Clinical Practice 120 (October 2016): S22. http://dx.doi.org/10.1016/s0168-8227(16)30939-1.

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