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Artykuły w czasopismach na temat „Intimal hyperplasia”

Autor: Grafiati

Data publikacji: 4 czerwca 2021

Data aktualizacji: 25 lipca 2025

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1

Yan, Huifang, Xiwei Peng, Hao Xu, Jiahuan Zhu, and Changqing Deng. "Inhibition of Aortic Intimal Hyperplasia and Vascular Smooth Muscle Proliferation and Extracellular Matrix Protein Expressions by Astragalus–Angelica Combination." Evidence-Based Complementary and Alternative Medicine 2018 (August 13, 2018): 1–15. http://dx.doi.org/10.1155/2018/1508637.

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VSMC proliferation and ECM deposition always resulted in intimal hyperplasia. Astragalus–Angelica combination has a protective effect on the cardiovascular system. The inhibition effect of different Astragalus–Angelica combination on the hyperplastic intima after vascular balloon injury in rats was investigated in this study. Astragalus–Angelica combination can inhibit the intima hyperplasia after balloon injury, in which a 1:1 ratio shows excellent results. Astragalus–Angelica combination can enhance the expression of smooth muscleα-actin (SMа-actin) and inhibit the expression of proliferatin

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ARPA, Abdurrahman, and Pınar AYDIN OZTURK. "Histopathological effects of nimodipine and pentoxifylline on the vessel wall in end-to-end anastomoses in rat carotid arteries." Journal of Experimental and Clinical Medicine 39, no. 3 (2022): 879–83. http://dx.doi.org/10.52142/omujecm.39.3.54.

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When reperfusion following ischemia occurs, oxygen returns to the ischemic tissue, increasing free oxygen radicals and inducing paradox secondary damage. Before infarction, revascularization may influence the morbidity rate. Successful revascularization is not always achieved due to stenosis incidence, proliferation of smooth muscle cells, and intimal hyperplasia. This study compares the effects of nimodipine that prevents vasospasm and pentoxifylline, which stimulates growth factors and reduces collagen synthesis on intimal hyperplasia. Eighteen randomly selected Sprague-Dawley rats were divi

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Hirai, T., Y. Korogi, M. Harada, and M. Takahashi. "Prevention of Intimal Hyperplasia by Irradiation." Acta Radiologica 37, no. 1P1 (1996): 229–33. http://dx.doi.org/10.1177/02841851960371p147.

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Purpose: This experimental study was designed to investigate the effect of irradiation in prevention of intimal hyperplasia. Material and Methods: Twenty rabbits were divided into 4 groups, which were irradiated with 2, 5, 10, and 20 Gy, respectively. The intima of both femoral arteries was injured by air-drying, and irradiation was performed on the unilateral side. The contralateral femoral artery served as a control. Angiograms as well as histologic specimens were obtained 1 month later. Results: Marked intimal hyperplasia was observed in all control sites. There were no significant differen

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Koshy, Prakash, Amanda Self, Philip J. Kadowitz, Vivian A. Fonseca, and Dennis B. McNamara. "Effects of low-dose candesartan on the rate of re-endothelialisation following vascular wound healing." Journal of the Renin-Angiotensin-Aldosterone System 2, no. 1_suppl (2001): S81—S83. http://dx.doi.org/10.1177/14703203010020011401.

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The wound healing response of the vascular wall to injury involves re-endothelialisation of the denuded luminal surface and thickening of the intimal area (intimal hyperplasia), as expressed by the intimal-to-medial area ratio (I/M). Candesartan, at doses of 1 mg/kg/day or higher, has been reported to attenuate the intimal hyperplastic response. We tested the hypothesis that candesartan, at doses lower than those associated with attenuation of intimal hyperplasia, may affect re-endothelialisation. New Zealand White rabbits were subjected to balloon catheter injury to the thoracic aorta. Candes

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5

Mesfin, G. M., M. J. Higgins, W. P. Brown, and D. Rosnick. "Cardiovascular Complications of Chronic Catheterization of the Jugular Vein in the Dog." Veterinary Pathology 25, no. 6 (1988): 492–502. http://dx.doi.org/10.1177/030098588802500613.

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Cardiovascular changes associated with indwelling catheters were evaluated in 51 adult beagle dogs catheterized for 4 to 9 weeks. Pathologic changes consistent with traumatic injury were in the vena cava and endocardium of the right atrium of 88% of cannulated dogs. Lesions were characterized by surface denudation and diffuse intimal thickening due to myointimal hyperplasia and deposition of extracellular matrix. Affected intima was lined by hyperplastic, poorly differentiated endothelial cells and contained round to oval cells with characteristics of smooth muscle cells. After 9 weeks, thicke

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6

Shiroma, H., and A. Kusaba. "Ultrastructural Features of Progressive Intimal Hyperplasia at the Distal End-to-Side Anastomosis of Vein Grafts." Cardiovascular Surgery 4, no. 3 (1996): 393–98. http://dx.doi.org/10.1177/096721099600400327.

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The features of intimal hyperplasia at the distal end-to-side anastomosis of arterially implanted autovein bypass grafts in dogs were examined using light and transmission electron microscopy. The bypass grafting was done under conditions of reduced blood flow with an abnormal flow wave and high peripheral resistance. Anastomotic intimal hyperplasia was evident 14 to 31 days after implantation, then gradually increased, particularly at the toe portion of the anastomosis. From 6 to 12 months after implantation, the intimal hyperplasia was excessively increased and severe luminal stenosis had de

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7

O'Malley, M. K. "Intimal hyperplasia." European Journal of Vascular Surgery 6, no. 4 (1992): 343–45. http://dx.doi.org/10.1016/s0950-821x(05)80277-4.

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8

Aydin, Unal, Murat Ugurlucan, Funda Gungor, et al. "Effects of Atorvastatin on Vascular Intimal Hyperplasia: An Experimental Rodent Model." Angiology 60, no. 3 (2008): 370–77. http://dx.doi.org/10.1177/0003319708321102.

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Introduction Vascular intimal hyperplasia is associated with increased mortality and morbidity. The authors investigated the effects of atorvastatin on vascular intimal hyperplasia. Materials and methods Rats were divided into 4 groups. Groups 1, 2, and 3 had experimental aortic injury and received intraperitoneal injection of atorvastatin, solvent, or 0.9% NaCl, respectively. Group 4 was a nonintervention (laparotomy only) control group. Animals were sacrificed after 3 weeks. Blood samples and injured aortic segment were analyzed. Results Atorvastatin administration significantly lowered tota

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9

Karasu, Aykut, Yılmaz Güler, Soner Büyükkınacı, and Halil Toplamoğlu. "Deneysel Karotis Endarterektomide “Abciximab”ın Restenozis Üzerine Etkisi." Sinir Sistemi Cerrahisi Dergisi 1, no. 1 (2008): 12–19. https://doi.org/10.54306/sscd.2008.43.

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Objective: Thrombosis and intimal hyperplasia occuring after carotid endarterectomy cause restonosis. By preventing activation of platelets and neointimal hyperplasia, carotid thrombosis and intimal hyperplasia can be impeded. In this study we applied platelet gpIIa/gpIIIb receptor blocker abciximab on rat vessel walls and examined its effect on intimal hyperplasia. Methods: Abciximab was produced at mammiferous cell culture as fab portion of 7E3 monoclonal antibody. It inhibits platelet aggregation by binding glicoprotein IIa/IIIb receptor on platelet. It also inhibits intimal hyperplasia by

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10

Bledsoe, Shelly L., Aliza T. Brown, Joseph A. Davis, Hongjiang Chen, John F. Eidt, and Mohammed M. Moursi. "Effect of Clopidogrel on Platelet Aggregation and Intimal Hyperplasia following Carotid Endarterectomy in the Rat." Vascular 13, no. 1 (2005): 43–49. http://dx.doi.org/10.1258/rsmvasc.13.1.43.

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Intimal hyperplasia results in significant morbidity and mortality following vascular intervention. Both platelets and elevated homocysteine have been implicated in the development of intimal hyperplasia. We previously demonstrated that a locally applied antiplatelet agent decreases the development of intimal hyperplasia. We were therefore interested in a systemic antiplatelet agent, clopidogrel. We hypothesized that clopidogrel would decrease platelet aggregation and activity and intimal hyperplasia. Male Sprague-Dawley rats underwent carotid endarterectomy (CEA) and treatment with either pla

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11

Jalaeefar, Amirmohsen, Arash Mohammadi Tofigh, Atoosa Gharib, Mohsen Khandaghy, and Mohammad Reza Rahimi. "Effects of N-acetylcysteine on arterial neo-intimal hyperplasia in rat model of arteriovenous fistula." Journal of Vascular Access 20, no. 2 (2018): 190–94. http://dx.doi.org/10.1177/1129729818793368.

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Introduction: Arteriovenous fistula is the best choice for vascular access in hemodialysis patients. However, arteriovenous fistula dysfunction is a major clinical issue. The most common cause of arteriovenous fistula failure is intimal hyperplasia. In this study, we have investigated the effect of N-acetylcysteine on neo-intimal hyperplasia after arteriovenous fistula creation in rats. Methods: This study was conducted in 24 rats which were randomly divided into two groups: control and N-acetylcysteine groups. An end-to-side anastomosis was made between the femoral artery and vein. The contro

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12

Chen, C., K. A. Coyle, J. D. Hughes, A. B. Lumsden, and D. N. Ku. "Reduced Blood Flow Accelerates Intimal Hyperplasia in Endarterectomized Canine Arteries." Cardiovascular Surgery 5, no. 2 (1997): 161–68. http://dx.doi.org/10.1177/096721099700500205.

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The purpose of this study was to evaluate a technique that accelerates intimal hyperplasia by reduction of blood flow. Bilateral endarterectomies were performed in both femoral and carotid arteries in six dogs. One week later, all animals underwent banding of an artery distal to the injured region to reduce the blood flow by 50%. The contralateral injured arteries served as controls. At 11 weeks, the specimens were harvested and analyzed. Five of 12 (42%) of the flow-restricted arteries and nine of 12 (75%) of the non-flow-restricted arteries were patent at 11 weeks ( P<0.05). Marked stenot

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13

Saroyan, R. M., M. P. Roberts, J. T. Light, et al. "Differential recovery of prostacyclin and endothelium-derived relaxing factor after vascular injury." American Journal of Physiology-Heart and Circulatory Physiology 262, no. 5 (1992): H1449—H1457. http://dx.doi.org/10.1152/ajpheart.1992.262.5.h1449.

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Differential recovery of prostacyclin and endothelium-derived relaxing factor after vascular injury. Am. J. Physiol. 262 (Heart Circ. Physiol. 31): H1449-H1457, 1992. The recovery of prostacyclin (prostaglandin I2, PGI2) synthesis and endothelium-derived relaxing factor (EDRF) activity, as demonstrated by acetylcholine (ACh)-induced relaxation, by rabbit aorta was examined up to 8 wk after balloon catheter-induced injury. Following injury, basal 6-keto-PGF1 alpha formation was decreased acutely; however, after 3 wk it was not different from control. Arachidonic acid-stimulated 6-keto-PGF1 alph

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14

Van Phung, Doan, Takeshi Kinoshita, Tohru Asai, and Tomoaki Suzuki. "Histological and Morphometric Properties of Skeletonized Gastroepiploic Artery and Risk Factors for Intimal Hyperplasia." Innovations: Technology and Techniques in Cardiothoracic and Vascular Surgery 7, no. 3 (2012): 191–94. http://dx.doi.org/10.1097/imi.0b013e318264f4cb.

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Objective The aim of the present study was to examine the histological and morphometric properties of skeletonized gastroepiploic artery (GEA) and the risk factors for intimal hyperplasia. Methods We obtained the redundant distal segments of skeletonized GEAs from 33 patients undergoing coronary bypass surgery and microscopically examined the transverse sections just distal to the most distal anastomoses. Intimal hyperplasia was evaluated on the basis of intima-to-media ratio and percentage of luminal narrowing. Risk factors were examined using multivariate linear regression analysis. Results

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Osgood, Michael J., Charles R. Flynn, Padmini Komalavilas, and Colleen Brophy. "Cell-permeant peptide inhibitors of vasospasm and intimal hyperplasia." Vascular 21, no. 1 (2012): 46–53. http://dx.doi.org/10.1258/vasc.2011.201203.

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Outcomes from vein graft bypass are limited by graft failure, leading causes of which include intimal hyperplasia and vasospasm. intimal hyperplasia remains the most common cause of graft failure, but no therapeutic modalities have been shown to prevent intimal hyperplasia in humans. The small heat shock proteins are a class of naturally occurring proteins in vascular smooth muscle. These proteins have an integral role in maintenance of vascular tone and in cellular defense against various stressors. Transduction domains have enabled intracellular therapeutic delivery of peptide analogs of hea

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Mitra, Amit K., Michael G. Del Core, and Devendra K. Agrawal. "Cells, cytokines and cellular immunity in the pathogenesis of fibroproliferative vasculopathies." Canadian Journal of Physiology and Pharmacology 83, no. 8-9 (2005): 701–15. http://dx.doi.org/10.1139/y05-080.

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Atherosclerosis and restenosis are the result of vascular injury followed by an inflammatory and fibroproliferative response that involves a large number of growth factors, cytokines, and cellular elements. Platelet activation and leukocyte recruitment into the arterial intima play a crucial role, initiating a whole spectrum of reactions leading to vascular smooth muscle cell hyperplasia and intimal migration. The roles of macrophages and lymphocytes and mast cells as mediators of inflammation and immune response is discussed, as are the roles of growth factors and cytokines. New light on the

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Hariri, R. J., D. R. Alonso, D. P. Hajjar, D. Coletti, and M. E. Weksler. "Aging and arteriosclerosis. I. Development of myointimal hyperplasia after endothelial injury." Journal of Experimental Medicine 164, no. 4 (1986): 1171–78. http://dx.doi.org/10.1084/jem.164.4.1171.

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Old Fischer 344 rats are more susceptible to vascular lesions after arterial endothelial injury than are young animals. Thus, 20-26-mo-old Fischer 344 rats developed greater and more persistent intimal proliferative lesions than did 2-5-mo-old rats after aortic endothelial denudation. 3 d after deendothelialization, intimal thickness was increased two-fold in both old and young animals. However, 14 d after endothelial injury, intimal thickness had increased nearly five times in old animals, but had regressed to normal in young animals. Intimal thickness of young aortic grafts transplanted into

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18

Kemahli, Mustafa Baris, Tugra Gencpinar, Huseyin Dursun, et al. "Effects Of Rivaroxaban And Apixaban On Intimal Hyperplasia In Rabbits." Turkish Journal of Vascular Surgery 31, no. 3 (2022): 148–56. http://dx.doi.org/10.9739/tjvs.2022.09.03.

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Aim: Intimal hyperplasia causes vascular occlusion and its optimal treatment is unknown. In this study, we evaluated the effectiveness of Apixaban and Rivaroxaban treatment for preventing intimal hyperplasia in rabbits. Material and Methods: The rabbits (n = 15) were randomly divided into three groups. Reanastomoses are applied to the carotid artery. All groups received 100 U/kg heparin sodium during the operation period. Group A (n = 5) as a control group had no medication. Group B (n = 5) was given Rivaroxaban 3 mg/kg/day. In-group C (n = 5) Apixaban was administered per orally 10 mg/kg. At

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Zhang, Dechuan, Tieying Yin, Feifei Du, et al. "EVALUATION OF INTIMAL HYPERPLASIA AND THROMBOSIS AFTER IMPLANTATION OF PLATELET GLYCOPROTEIN IIIa MONOCLONAL ANTIBODY-ELUTING STENT IN NEW ZEALAND WHITE RABBIT AORTA OR ILIAC ARTERIES." Biomedical Engineering: Applications, Basis and Communications 27, no. 05 (2015): 1550046. http://dx.doi.org/10.4015/s1016237215500465.

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Since the percutaneous coronary intervention (PCI) was first introduced into China in 1984, this procedure has become widely accepted as an important step in coronary revascularization. This study aims to evaluate intimal hyperplasia and thrombosis after implantation of platelet glycoprotein IIIa monoclonal antibody (mAb)-eluting stent in the New Zealand white rabbit abdominal aorta or iliac artery by comparing CT angiography and pathological experiments. The antibody-eluting stents were prepared by the passive absorption method. Arterial intima in the stented segment and 0.5 cm adjacent to th

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Liang, Yuxin, and Yanlong Zhao. "Exploration of the Mechanism of Intimal Hyperplasia in Autogenous Arteriovenous Fistula." Journal of Contemporary Medical Practice 7, no. 1 (2025): 186–91. https://doi.org/10.53469/jcmp.2025.07(01).35.

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Objective: To explore the mechanism of intimal hyperplasia (IH) in autogenous arteriovenous fistula (AVF) from the perspective of integrated traditional Chinese and western medicine. Methods: This study reviewed the relevant literature, analyzed and summarized the mechanism of intimal hyperplasia of autogenous arteriovenous fistula from the perspective of integrated traditional Chinese and western medicine. Conclusion: Intimal hyperplasia of autogenous arteriovenous fistula involves many aspects. From any Angle, it provides a theoretical basis for clinical research and further guides clinical

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Galarza-Delgado, D. Á., J. R. Azpiri-López, I. J. Colunga-Pedraza, et al. "AB1212 PREVALENCE OF CAROTID SUBCLINICAL ATHEROSCLEROSIS IN PATIENTS WITH PSORIATIC ARTHRITIS VS RHEUMATOID ARTHRITIS: A CASE CONTROL STUDY." Annals of the Rheumatic Diseases 79, Suppl 1 (2020): 1897. http://dx.doi.org/10.1136/annrheumdis-2020-eular.5197.

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Background:Rheumatic diseases such as Psoriatic Arthritis (PsA) and Rheumatoid Arthritis (RA) are associated with increased morbidity and mortality, mainly due to cardiovascular causes. Cardiovascular outcomes in patients with PsA and RA cannot be completely explained by traditional cardiovascular risk factors, suggesting that the systemic inflammation that characterizes these diseases may have an important role on accelerated atherosclerosis.1Objectives:To compare carotid intima-media thickness (cIMT) and asymptomatic carotid plaque (CP) prevalence, between patients with PsA, RA and controls.

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Van der Geest, K., F. Borg, K. Wolfe, W. A. Schmidt, R. Luqmani, and B. Dasgupta. "FRI0195 ULTRASONOGRAPHIC HALO SCORE ASSOCIATES WITH INTIMAL HYPERPLASIA IN GIANT CELL ARTERITIS." Annals of the Rheumatic Diseases 79, Suppl 1 (2020): 680.3–681. http://dx.doi.org/10.1136/annrheumdis-2020-eular.2963.

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Background:We have recently developed a novel ultrasonographic Halo Score to quantify the extent of vascular inflammation in GCA [1]. High Halo Scores were associated with a high rate of ocular ischaemia among patients with GCA. Earlier studies have shown that GCA patients with intimal hyperplasia in their temporal artery biopsy (TAB) are at the highest risk of neuro-ophthalmic, ischaemic complications [2,3]. We therefore questioned whether the ultrasonographic Halo Score might be linked to the presence of intimal hyperplasia in patients with GCA.Objectives:To investigate the relationship betw

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Allon, Michael, Silvio H. Litovsky, Yingying Zhang, Ha Le, Alfred K. Cheung, and Yan-Ting Shiu. "Association of Preexisting Arterial Intimal Hyperplasia with Arteriovenous Fistula Outcomes." Clinical Journal of the American Society of Nephrology 13, no. 9 (2018): 1358–63. http://dx.doi.org/10.2215/cjn.13431217.

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Background and objectivesPreoperative arterial function is associated with arteriovenous fistula (AVF) development. Because arterial pathology may correlate with its function, preexisting arterial intimal hyperplasia may be associated with AVF development.Design, setting, participants, & measurementsVascular specimens obtained from 125 patients (with minimal 2 mm arterial diameter and 2.5 mm venous diameter) undergoing AVF creation were quantified for arterial intimal hyperplasia, arterial medial fibrosis, arterial microcalcification, and venous intimal hyperplasia. A 6-week postoperative

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Nakagawa, H., K. Kichikawa, K. Takayama, et al. "Palmaz Stent Deployment for Subclavian and Brachiocephalic Arterial Occlusive Disease." Interventional Neuroradiology 7, no. 1_suppl (2001): 49–52. http://dx.doi.org/10.1177/15910199010070s106.

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Palmaz stent deployment is a useful method for subclavian and brachiocephalic arterial occlusive disease. We evaluated restenosis or intimal thickening after Palmaz stent deployment for nine lesions of subclavian or brachiocephalic arterial occlusive disease focusing on stent diameter, atheroma thickness near the stent, and degree of coverage for the lesion. Follow up DSA and IVUS at 5–14 months (mean 9) after therapy showed no significant changes in the size or shape of the stent itself. There were two lesions of thin in-stent intimal hyperplasia and five lesions of thick hyperplasia. There w

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Brody, Jerome I., and Nancy J. Pickering. "Pathobiology of intimal hyperplasia." Journal of Vascular Surgery 10, no. 5 (1989): 585–87. http://dx.doi.org/10.1016/0741-5214(89)90154-7.

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Haudenschild, Christian C. "Morphology of intimal hyperplasia." Journal of Vascular Surgery 10, no. 5 (1989): 591–92. http://dx.doi.org/10.1016/0741-5214(89)90157-2.

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Levitt, Adam B., Keith Robinson, Eric Wellons, et al. "Prevention of intimal hyperplasia." Cardiovascular Radiation Medicine 5, no. 1 (2004): 34–37. http://dx.doi.org/10.1016/j.carrad.2004.03.002.

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Davies, M. G., and P. O. Hagen. "Pathobiology of intimal hyperplasia." British Journal of Surgery 81, no. 9 (1994): 1254–69. http://dx.doi.org/10.1002/bjs.1800810904.

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Sottiurai, V. S. "Can Intimal Hyperplasia and Distal Anastomotic Intimal Hyperplasia be Controlled and Prevented?" Annals of Vascular Surgery 21, no. 3 (2007): 289–91. http://dx.doi.org/10.1016/j.avsg.2007.03.001.

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Pyo, Robert, Yuichiro Sato, Nigel Mackman, and Mark Taubman. "Mice deficient in tissue factor demonstrate attenuated intimal hyperplasia in response to vascular injury and decreased smooth muscle cell migration." Thrombosis and Haemostasis 92, no. 09 (2004): 451–58. http://dx.doi.org/10.1160/th04-02-0122.

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SummaryTissue factor (TF) is the primary initiator of the coagulation cascade and is thought to play a key role in the generation of arterial thrombosis. Recent studies have suggested that TF mediates inflammatory processes in the arterial wall and may be an important regulator of intimal hyperplasia. We have employed genetically engineered mice (mTF−/−/hTF+) with markedly diminished TF activity (≈1% normal levels) to examine the role of TF in mediating the response to arterial injury. mTF−/−/hTF+ displayed a marked reduction in intimal hyperplasia (46% decrease in intimal area, 60% decrease i

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Hollingsworth, S. J., C. B. Tang, and S. G. E. Barker. "The Effects of Heparin on Cultured Explants of Varicose Long Saphenous Vein." Phlebology: The Journal of Venous Disease 16, no. 2 (2001): 60–67. http://dx.doi.org/10.1177/026835550101600203.

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Objective: To examine the effects of heparin on smooth muscle cells (SMCs) in explants of varicose, long saphenous vein (LSV). Procedures: Explants of varicose LSV were cultured for 7 days either alone, or with heparin at 10, 100 or 1000 IU/ml (Monoparin). At 7 days, cultured explants were analysed for changes in intimal and medial thickness and by immuno-histochemistry. Comparisons were made with explants at initial isolation and with similar, cultured explants of normal LSV. Results: In normal LSV, by day 7, SMC-derived neo-intimal hyperplasia developed ( p<0.01) with an increase in intim

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Che Man, Rohaina, Nadiah Sulaiman, Mohamad Fikeri Ishak, Ruszymah Bt Hj Idrus, Mohd Ramzisham Abdul Rahman, and Muhammad Dain Yazid. "The Effects of Pro-Inflammatory and Anti-Inflammatory Agents for the Suppression of Intimal Hyperplasia: An Evidence-Based Review." International Journal of Environmental Research and Public Health 17, no. 21 (2020): 7825. http://dx.doi.org/10.3390/ijerph17217825.

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Anti-atherogenic therapy is crucial in halting the progression of inflammation-induced intimal hyperplasia. The aim of this concise review was to methodically assess the recent findings of the different approaches, mainly on the recruitment of chemokines and/or cytokine and its effects in combating the intimal hyperplasia caused by various risk factors. Pubmed and Scopus databases were searched, followed by article selection based on pre-set inclusion and exclusion criteria. The combination of keywords used were monocyte chemoattractant protein-1 OR MCP-1 OR TNF-alpha OR TNF-α AND hyperplasia

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Zhang, Bao-fu, Zi-heng Wu, Jie Deng та ін. "M⁶A methylation-mediated elevation of SM22α inhibits the proliferation and migration of vascular smooth muscle cells and ameliorates intimal hyperplasia in type 2 diabetes mellitus". Biological Chemistry 403, № 3 (2021): 317–29. http://dx.doi.org/10.1515/hsz-2021-0296.

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Abstract Abnormal proliferation of vascular smooth muscle cells (VSMCs) induced by insulin resistance facilitates intimal hyperplasia of type 2 diabetes mellitus (T2DM) and N6-methyladenosine (m6A) methylation modification mediates the VSMC proliferation. This study aimed to reveal the m6A methylation modification regulatory mechanism. In this study, m6A demethylase FTO was elevated in insulin-treated VSMCs and T2DM mice with intimal injury. Functionally, FTO knockdown elevated m6A methylation level and further restrained VSMC proliferation and migration induced by insulin. Mechanistically, FT

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Kleinert, Leigh B., James B. Hoying, and Stuart K. Williams. "The Neointima Formed in Endothelial Cell Sodded ePTFE Vascular Grafts Results from Both Cellular-Hyperplasia and Extracellular-Hypertrophy." Cell Transplantation 5, no. 4 (1996): 475–82. http://dx.doi.org/10.1177/096368979600500406.

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Endothelial cell transplantation onto polymeric vascular grafts results in the formation of a neointima. The formation of this neointima is often suggested to result from a chronic cellular hyperplasia where the terms intimal hyperplasia and intimal thickening are used interchangeably. While the formation of a midgraft neointima in sodded grafts involves a level of cell proliferation, the synthesis and deposition of extracellular matrix proteins is also a ubiquitous observation in these grafts. To assess the composition of midgraft neointima in sodded grafts, a morphometric method was develope

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Light, J. T., J. A. Bellan, I. L. Chen, et al. "Angiopeptin enhances acetylcholine-induced relaxation and inhibits intimal hyperplasia after vascular injury." American Journal of Physiology-Heart and Circulatory Physiology 265, no. 4 (1993): H1265—H1274. http://dx.doi.org/10.1152/ajpheart.1993.265.4.h1265.

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The effects of the somatostatin analogue, angiopeptin (BIM-23014), on neoendothelial function, as evidenced by formation of prostaglandin (PG) I2 and by acetylcholine-induced relaxation (formation of endothelial-derived relaxing factor), were investigated in the rabbit aorta. A balloon catheter injury of the thoracic and abdominal aorta was induced in New Zealand White rabbits. Animals treated with angiopeptin for 2 or 4 wk were compared with untreated rabbits at 2 or 4 wk after the induction of injury, as well as to sham-operated controls. When the rabbits were killed, vascular rings were ass

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Wang, Yung-Chun, Dunpeng Cai, Xiao-Bing Cui, Ya-Hui Chuang, William P. Fay, and Shi-You Chen. "Janus Kinase 3 Deficiency Promotes Vascular Reendothelialization—Brief Report." Arteriosclerosis, Thrombosis, and Vascular Biology 41, no. 6 (2021): 2019–26. http://dx.doi.org/10.1161/atvbaha.121.316293.

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Objective: The objective of this study is to determine the role of JAK3 (Janus kinase 3) in reendothelialization after vascular injury. Methods and Results: By using mouse carotid artery wire injury and rat balloon injury model, we found that JAK3 regulates reendothelialization and endothelial cell proliferation after vascular injury. JAK3 and phospho-JAK3 levels were increased in neointimal smooth muscle cells in response to vascular injury in mice. JAK3 deficiency dramatically attenuated the injury-induced intimal hyperplasia in carotid arteries of both male and female mice. Importantly, JAK

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Asfar, Sami, Ali Shuaib, Fatemah Al-Otaibi, Sora S. Asfar, and Narayana Kilarkaje. "A New Technique to Induce Experimental Myointimal Hyperplasia." Medical Principles and Practice 27, no. 5 (2018): 415–19. http://dx.doi.org/10.1159/000492575.

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Background: Arterial myointimal hyperplasia (MIH) has a significant impact on the long-term outcomes of vascular procedures such as bypass surgery and angioplasty. In this study, we describe a new and innovative technique to induce MIH using a dental flossing cachet in Wistar rats. Methods: The intimal damage in the common carotid artery was induced by inserting the tip of the dental flossing cachet through the external carotid artery into the common carotid artery and turning it on for 3 rounds of 20 s each (n = 10). After 2 weeks, the rats were anesthetized and the common carotid arteries of

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Todorov, S. S., R. V. Sidorov, E. P. Talalaev, and I. F. Shlyk. "The role of glycosaminoglycanes in the development of intimal hyperplasia in the shunting of coronary arteries." Medical Herald of the South of Russia 9, no. 3 (2018): 94–98. http://dx.doi.org/10.21886/2219-8075-2018-9-3-94-98.

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The article is devoted to the study of the role of glycosaminoglycans (hyaluronic acid, heparan sulfate derivatives, dermatan sulfate) in the genesis of intimal arterial hyperplasia. It is shown that these substances play important role in the structural reorganization of vessels, including the development of intimal hyperplasia of the arteries. Scientific works on the role of GAG in the genesis of intimal hyperplasia are based on experimental data. The authors draw attention to GAG involvement in cell-intercell nteractions of artery walls, including proliferation, migration, signal transducti

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Hui, David. "Intimal Hyperplasia in Murine Models." Current Drug Targets 9, no. 3 (2008): 251–60. http://dx.doi.org/10.2174/138945008783755601.

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HOOD, PHYLLIS B. "An Overview of Intimal Hyperplasia." Radiology 180, no. 2 (1991): 378. http://dx.doi.org/10.1148/radiology.180.2.378.

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Mills, B., T. Robb, and DF Larson. "Intimal hyperplasia: slow but deadly." Perfusion 27, no. 6 (2012): 520–28. http://dx.doi.org/10.1177/0267659112452316.

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Rose, Marlene L. "Interferon-γ and Intimal Hyperplasia". Circulation Research 101, № 6 (2007): 542–44. http://dx.doi.org/10.1161/circresaha.107.160911.

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Lee, Samuel, and Richard T. Lee. "Mechanical Stretch and Intimal Hyperplasia." Arteriosclerosis, Thrombosis, and Vascular Biology 30, no. 3 (2010): 459–60. http://dx.doi.org/10.1161/atvbaha.109.201509.

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Lemson, M. S., J. H. M. Tordoir, M. J. A. P. Daemen, and P. J. E. H. M. Kitslaar. "Intimal Hyperplasia in Vascular Grafts." European Journal of Vascular and Endovascular Surgery 19, no. 4 (2000): 336–50. http://dx.doi.org/10.1053/ejvs.1999.1040.

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Greisler, Howard P. "Vascular prosthesis/healing/intimal hyperplasia." Journal of Vascular Surgery 20, no. 1 (1994): 131–32. http://dx.doi.org/10.1016/0741-5214(94)90193-7.

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LaMuraglia, Glenn M. "Pharmacologic suppression of intimal hyperplasia." Journal of Vascular Surgery 20, no. 6 (1994): 1010–11. http://dx.doi.org/10.1016/0741-5214(94)90247-x.

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Gibbons, Gary H. "Restenosis: Remodeling Versus Intimal Hyperplasia." Journal of Vascular and Interventional Radiology 7, no. 1 (1996): 55–62. http://dx.doi.org/10.1016/s1051-0443(96)70027-1.

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Bundens, W. P., and Y. Wolf. "The etiology of intimal hyperplasia." Medical Hypotheses 43, no. 5 (1994): 343–46. http://dx.doi.org/10.1016/0306-9877(94)90114-7.

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Newby, Andrew C., and Alla B. Zaltsman. "Molecular mechanisms in intimal hyperplasia." Journal of Pathology 190, no. 3 (2000): 300–309. http://dx.doi.org/10.1002/(sici)1096-9896(200002)190:3<300::aid-path596>3.0.co;2-i.

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IKEGAYA, NAOKI, TATSUO YAMAMOTO, AKIHIRO TAKESHITA та ін. "Elevated Erythropoietin Receptor and Transforming Growth Factor-β1 Expression in Stenotic Arteriovenous Fistulae Used for Hemodialysis". Journal of the American Society of Nephrology 11, № 5 (2000): 928–35. http://dx.doi.org/10.1681/asn.v115928.

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Abstract. The issue of whether recombinant human erythropoietin (rhEPO) increases thrombosis of arteriovenous (AV) fistulae used for hemodialysis remains unclear. Thrombosis often occurs at stenotic segments of fistulae where there is marked intimal hyperplasia and extracellular matrix accumulation. Increased expression of transforming growth factor-β1 (TGF-β1) has been shown to be involved in the development of atherosclerotic lesions by promoting intimal hyperplasia and extracellular matrix accumulation. To clarify the role of rhEPO in the development of stenosis of AV fistulae, this study e

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