Littérature scientifique sur le sujet « PATHOLOGICAL VASCULAR REMODELING »
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Articles de revues sur le sujet "PATHOLOGICAL VASCULAR REMODELING"
Ali, Zaheer, Anthony Mukwaya, Antje Biesemeier, Maria Ntzouni, Daniel Ramsköld, Sarantis Giatrellis, Parviz Mammadzada et al. « Intussusceptive Vascular Remodeling Precedes Pathological Neovascularization ». Arteriosclerosis, Thrombosis, and Vascular Biology 39, no 7 (juillet 2019) : 1402–18. http://dx.doi.org/10.1161/atvbaha.118.312190.
Texte intégralUemura, Y., R. Shibata, K. Ohashi, T. Enomoto, Y. Kataoka, M. Miyabe, D. Yuasa, K. Matsuo, N. Ouchi et T. Murohara. « An adipokine omentin prevents pathological vascular remodeling ». European Heart Journal 34, suppl 1 (2 août 2013) : P597. http://dx.doi.org/10.1093/eurheartj/eht307.p597.
Texte intégralHan, Yue, Kai Huang, Qing-Ping Yao et Zong-Lai Jiang. « Mechanobiology in vascular remodeling ». National Science Review 5, no 6 (26 décembre 2017) : 933–46. http://dx.doi.org/10.1093/nsr/nwx153.
Texte intégralWang, Zheng, Xiao Wu, Jiali Li, Qiru Guo, Zhong Jin, Hongfei Li, Bing Liang et al. « Potassium Dehydroandrograpolide Succinate Targets NRP1 Mediated VEGFR2/VE-Cadherin Signaling Pathway to Promote Endothelial Barrier Repair ». International Journal of Molecular Sciences 24, no 4 (4 février 2023) : 3096. http://dx.doi.org/10.3390/ijms24043096.
Texte intégralJia, Zhuangzhuang, Shuai Wang, Haifeng Yan, Yawen Cao, Xuan Zhang, Lin Wang, Zeyu Zhang, Shanshan Lin, Xianliang Wang et Jingyuan Mao. « Pulmonary Vascular Remodeling in Pulmonary Hypertension ». Journal of Personalized Medicine 13, no 2 (19 février 2023) : 366. http://dx.doi.org/10.3390/jpm13020366.
Texte intégralChan, Stefan, et Chen Yan. « PDE1 isozymes, key regulators of pathological vascular remodeling ». Current Opinion in Pharmacology 11, no 6 (décembre 2011) : 720–24. http://dx.doi.org/10.1016/j.coph.2011.09.002.
Texte intégralEsteban, Vanesa, Nerea Méndez-Barbero, Luis Jesús Jiménez-Borreguero, Mercè Roqué, Laura Novensá, Ana Belén García-Redondo, Mercedes Salaices et al. « Regulator of calcineurin 1 mediates pathological vascular wall remodeling ». Journal of Experimental Medicine 208, no 10 (19 septembre 2011) : 2125–39. http://dx.doi.org/10.1084/jem.20110503.
Texte intégralEsteban, Vanesa, Nerea Méndez-Barbero, Luis Jesús Jiménez-Borreguero, Mercè Roqué, Laura Novensá, Ana Belén García-Redondo, Mercedes Salaices et al. « Regulator of calcineurin 1 mediates pathological vascular wall remodeling ». Journal of Cell Biology 195, no 1 (3 octobre 2011) : i1. http://dx.doi.org/10.1083/jcb1951oia11.
Texte intégralHong, Xuechong, et Wenduo Gu. « Plasticity of vascular resident mesenchymal stromal cells during vascular remodeling ». Vascular Biology 1, no 1 (12 août 2019) : H67—H73. http://dx.doi.org/10.1530/vb-19-0022.
Texte intégralJin, Xin, Guo-xiang Fu, Xiao-dong Li, Ding-liang Zhu et Ping-jin Gao. « Expression and Function of Osteopontin in Vascular Adventitial Fibroblasts and Pathological Vascular Remodeling ». PLoS ONE 6, no 9 (19 septembre 2011) : e23558. http://dx.doi.org/10.1371/journal.pone.0023558.
Texte intégralThèses sur le sujet "PATHOLOGICAL VASCULAR REMODELING"
Hendel, Alon. « Granzyme B in vascular remodeling and pathological angiogenesis ». Thesis, University of British Columbia, 2013. http://hdl.handle.net/2429/44782.
Texte intégralMinami, Takeya. « Reciprocal expression of MRTF-A and myocardin is crucial for pathological vascular remodeling in mice ». Kyoto University, 2013. http://hdl.handle.net/2433/174774.
Texte intégralKeuylian, Zela Talar. « The implication of adenylyl cyclase isoform 8 and its regulation by the Notch pathway in vascular smooth muscle cell transdifferentiation and pathological vesel remodeling ». Paris 6, 2013. http://www.theses.fr/2013PA066110.
Texte intégralAtherosclerosis is characterized by the narrowing of the arterial lumen termed “stenosis”, due to the expansion of arterial plaques. One of the major contributing factors to the formation of lesions and the neo-intima during post-angioplasty restenosis is the phenotypic change of medial vascular smooth muscle cells. This process switches them from a quiescent/contractile phenotype to a secretory, proliferative, migratory one. My work consisted of elucidating some of the molecular mechanisms implicated in this switch. We showed that the expression of an adenylyl cyclase (AC) isoform, AC8, is implicated in both the inflammatory and migratory properties acquired by trans-differentiated VSMCs. In human atherosclerotic arteries we showed that only intimal VSMCs strongly express AC8; very few AC8 positive VSMCs were detected in the medial layer, either in atherosclerotic or healthy arteries. In the rat balloon injury model of restenosis, we showed a transitory increase of AC8 expression. In vitro, we demonstrated that AC8 expression is regulated by the Notch pathway; inhibiting Notch amplified AC8 expression and decreased Notch target genes Hrt1 and Hrt3. In the same model of restenosis, the transitory up-regulation of AC8 expression coincided with Notch3 down-regulation. These set of experiments demonstrated that the Notch pathway decreases IL1β-mediated AC8 up-regulation in trans-differentiated VSMCs and suggests that AC8 expression, besides being induced by the proinflammatory cytokine IL1β,also depends on the down-regulation of the Notch pathway occurring in an inflammatory context. As a whole, my studies attribute a new role for AC8 in pathological vascular remodeling
Hsieh, Nan-Kuang, et 謝楠光. « Vascular Pathological Changs and Remodeling In Various Segments of Cerebral Arteries Following Chronic Nitric Oxide Blockade : A Comparison Between Hypertensive and Normotensive Rats ». Thesis, 2004. http://ndltd.ncl.edu.tw/handle/38443779512911708563.
Texte intégral國防醫學院
醫學科學研究所
92
Stroke and coronary arterial disease are two major cardiovas-cular events in hypertensive patients. Cerebrovascular diseases and stroke remain the main causes of mortality and morbidity in elderly hypertensive patients. Eedogenous nitric oxide (NO) exerts critical and diverse functions in the cardiovascular system, and abnormalities in NO production is associated with a number of cardiovascular diseases. In a series of studies, we carried out the analysis of blood pressure and vascular structure in spontaneously hypertensive rats(SHR)and normotensive Wistar-Kyoto strain(WKY)following chronic blockade of nitric oxide synthase (NOS) with Nω-nitro- L-arginine methyl ester (L-NAME). The aim of these studies were to evaluate the vascular remodelling of cerebral arteries following L-NAME in SHR and WKY.Five-wk-old male WKY and SHR were given with L-NAME (1 mg/ml) from 5th to 7th or 9th wk. The vascular remodelling and arteriolar injury score (AIS) in cerebral artery beds were assessed by various staining techniques. In WKY and SHR, L-NAME caused time-dependent elevations in tail cuff pressure (TCP) which represents the systolic arterial pressure. In SHR, L-NAME decreased body weight, but increased heart weight. The magnitude of TCP increase was much larger in SHR than WKY(+81.0±3.2 mmHg vs.+30.0±2.2 mmHg; p<0.01). The lumen diameter and media area of internal carotid artery (ICA) in hypertensive rats were smaller than those in untreated-WKY. These findings indicate that cerebral vascular remodelling occurs following chronic hyper- tension resulted from either genetic origin or NO deprivation. L-NAME significantly increased the media thickness in SHR, but not in WKY. Arteriolar hyalinosis and AIS in various segments of CA were assessed with periodic acid-Schiff staining and inflammatory cells were immuno- stained with the antibody against macrophage/monocyte marker (ED1). This agent also caused increase in cell volume density, AIS, inflammatory cells infiltration in perivascular space and negative growth index in ICA. The media/lumen ratio was higher in SHR than WKY, and further increased following L-NAME treatment. Diversified vascular remodelling occurred in hypertensive rats, but not in untreat-ed-WKY. These results suggest that NO deprivation and genetic hypertension cause morphological changes in various segments of cerebral arteries. ED1 positive (ED1+)cells appeared in the middle cerebral arteries of L- NAME-SHR as early as 2 wks after treatment. These cells were not observed in L-NAME-WKY and untreated-SHR. More ED1+ cells were found in L-NAME-SHR than L-NAME-WKY after 4-wk. AIS and the number of ED1+ cells around perivascular area of internal carotid artery were significantly higher in L-NAME treated rats (AIS: 137±28 in L-NAME-WKY vs 46±10 in Untreated-WKY, 169±18 in L-NAME-SHR vs 53±6 in untreated-SHR; p<0.01. ED1+ cells: 7.9 ±0.6 in L-NAME-WKY vs 1.3±0.9 in untreated-WKY, 13.6±2.7 in L-NAME-SHR vs 2.1±0.9 in Untreated-SHR; p<0.01), although TCP was higher in untreated-SHR than L-NAME-WKY(170±4 vs 137±4 mmHg; p<0.05). L-NAME significantly reduced blood flow. In low-flow states, accentuated pro-duction of mitogenic and fibrogenic growth factors such as platelet-derived growth factor and transforming growth factor-βprobably mediates inward remodelling by increas-ing smooth muscle cell hypertrophy and fibronectin deposition, whereas metalloproteinase induction provides reorganization of vessel structure. The mechanisms of decreased body weight may be L-NAME increases plasma renin activity and inhibited renin release. L-NAME attenuated the natriuresis, diuresis, and decreased proximal tubular resorption that normally accompany acute isotonic expansion of extracellular fluid volume. The mechanisms of increased heart weight may involve higher systolic blood pressure, plasma rennin activity and cardiac angiotensin converting enzyme activity in L-NAME rats than those of the subgroup without treatment of L-NAME. The hemo- dynamic load imposed on the heart is due not only to the level of blood pressure but also to concomitant hemodynamic volume load, arterial stiffness, and other factors. The hypothesis of mechanism of cardiac and vascular changes following the treatment with L-NAME might be cellular hyper- trophy due to increase inflammatory cells and proteins and apoptosis and body weight decreased due to the volume of extra- cellular fluid and interstitial components. Our study has two major findings: One is vascular cellular hypertrophy with Medial hypotrophy in L-NAME rats, besides medial thickness and cellular hypertrophy. The other is inflammatory cells expression in adventitial layer of vessels in L-NAME rats, not in subendothelial layer and untreaed-SHR. These findings suggest that ED1+ cells appeared in the middle cerebral arteries of L-NAME-SHR as early as 2 wks after treatment. Chronic inhibition of NO accelerates hypertension and induces perivascular inflammation. These important results may provide information to the mechanisms and risk factors leading to stroke.
PACCOSI, SARA. « CARATTERIZZAZIONE DI CELLULE DENDRITICHE UMANE NEL RIMODELLAMENTO VASCOLARE PATOLOGICO PER L'INDIVIDUAZIONE DI BERSAGLI FARMACOLOGICI ». Doctoral thesis, 2013. http://hdl.handle.net/2158/796857.
Texte intégralMaio, Twofoot Maria Tina. « CLINICAL AND EXPERIMENTAL EVIDENCE FOR THE PATHOLOGICAL MECHANISMS UNDERLYING ASPECTS OF SEXUAL DYSFUNCTION : IMPACT OF ADIPOSITY AND CHRONIC KIDNEY DISEASE ». Thesis, 2013. http://hdl.handle.net/1974/8366.
Texte intégralThesis (Ph.D, Pharmacology & Toxicology) -- Queen's University, 2013-09-30 22:33:20.436
Livres sur le sujet "PATHOLOGICAL VASCULAR REMODELING"
1945-, Hori M., Janicki Joseph S et Maruyama Yukio 1941-, dir. Cardiac-vascular remodeling and functional interaction. Tokyo : Springer, 1997.
Trouver le texte intégralHori, Masatsugu, Yukio Maruyama et Joseph S. Janicki. Cardiac-Vascular Remodeling and Functional Interaction. Springer London, Limited, 2013.
Trouver le texte intégralMaruyama, Yukio. Cardiac-Vascular Remodeling and Functional Interaction. Springer, 2013.
Trouver le texte intégralHori, Masatsugu, Yukio Maruyama et Joseph S. Janicki. Cardiac-Vascular Remodeling and Functional Interaction. Springer, 2014.
Trouver le texte intégralYang, Zhihong, et Xiu-Fen Ming. Adventitia and perivascular adipose tissue—the integral unit in vascular disease. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198755777.003.0020.
Texte intégralChapitres de livres sur le sujet "PATHOLOGICAL VASCULAR REMODELING"
Kawashima, Seinosuke, Ken-ichi Hirata et Mitsuhiro Yokoyama. « Nitric Oxide and the Heart : Implications in Physiological and Pathological Conditions ». Dans Cardiac-Vascular Remodeling and Functional Interaction, 367–79. Tokyo : Springer Japan, 1997. http://dx.doi.org/10.1007/978-4-431-67041-4_28.
Texte intégralCui, Jiaxin, Mariluz Rojo Domingo, Ryan Konno, Claudia A. Manetti, George Kagugube, Oscar Odeigah et Joakim Sundnes. « Impact of Pathological Vascular Remodelling on Right Ventricular Mechanics ». Dans Computational Physiology, 91–109. Cham : Springer Nature Switzerland, 2023. http://dx.doi.org/10.1007/978-3-031-25374-4_7.
Texte intégralRenna, Nicolas F., Rodrigo Garcia, Jesica Ramirez et Roberto M. Miatello. « Vascular Repair and Remodeling : A Review ». Dans Physiologic and Pathologic Angiogenesis - Signaling Mechanisms and Targeted Therapy. InTech, 2017. http://dx.doi.org/10.5772/67485.
Texte intégralRobinson, Chapman. « Pulmonary hypertension (PHT) ». Dans Oxford Handbook of Respiratory Medicine, sous la direction de Stephen J. Chapman, Grace V. Robinson, Rahul Shrimanker, Chris D. Turnbull et John M. Wrightson, 449–66. Oxford University Press, 2021. http://dx.doi.org/10.1093/med/9780198837114.003.0038.
Texte intégralActes de conférences sur le sujet "PATHOLOGICAL VASCULAR REMODELING"
Song Hu. « Multi-parametric photoacoustic microscopy of pathological remodeling in vascular anatomy and function ». Dans 2015 IEEE Photonics Conference (IPC). IEEE, 2015. http://dx.doi.org/10.1109/ipcon.2015.7323619.
Texte intégralMcGah, Patrick M., Alberto Aliseda, Daniel F. Leotta et Kirk W. Beach. « Effects of Wall Distensibility on the Numerical Simulation of Arteriovenous Fistulae ». Dans ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14183.
Texte intégralSheidaei, A., S. C. Hunley, L. G. Raguin et S. Baek. « Simulation of Aneurysm Growth With Stepwise Updating of Hemodynamic Loads Using an MRI-Based Geometric Model ». Dans ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-205499.
Texte intégralBaek, Seungik, C. Alberto Figueroa, Charles A. Taylor et Jay D. Humphrey. « A Framework for Fluid-Solid-Growth Modeling and its Application to Understanding the Enlargement of a Fusiform Aneurysm ». Dans ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-192805.
Texte intégralHaskett, Darren, Marie Fouts, Urs Utzinger, Doug Larson, Mohamad Azhar et Jonathan Vande Geest. « The Effects of Angiotensin II Infusion on the Mechanical Response and Microstructural Organization of Mouse Aorta ». Dans ASME 2010 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/sbc2010-19635.
Texte intégralGraham, BB, L. Zhang, MM Mentink-Kane, H. El-Haddad, HS Champion, TA Wynn, G. Butrous et RM Tuder. « Physiologic and Pathologic Analysis of a Murine Model of Schistosomiasis Pulmonary Vascular Remodeling. » Dans American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a1796.
Texte intégralCoyle, K., M. Ratsep, K. Laverty, M. M. Vandenbroek, L. R. Hilton, M. Mitchell, Y. Deng, D. J. Stewart, E. Vivier et M. L. Ormiston. « Natural Killer Cell TGFβ Signalling Influences Pulmonary Vascular Development and Pathological Vascular Remodelling in a Mouse Model of Pulmonary Arterial Hypertension ». Dans American Thoracic Society 2022 International Conference, May 13-18, 2022 - San Francisco, CA. American Thoracic Society, 2022. http://dx.doi.org/10.1164/ajrccm-conference.2022.205.1_meetingabstracts.a4723.
Texte intégralLiu, Fei, Margarita M. Suarez Velandia, Emeka Ifedigbo, Aleksandar Marinkovic, Xiaoli Liu, Daniel J. Tschumperlin et Laura E. Fredenburgh. « Pathologic Matrix Stiffening Promotes Cyclooxygenase (COX)-2-Dependent Mechanobiological Feedback Amplification Of Vascular Remodeling In Pulmonary Arterial Hypertension ». Dans American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a2622.
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