2012
DOI: 10.3389/fgene.2012.00290
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Mechanisms of arterial remodeling: lessons from genetic diseases

Abstract: Vascular disease is still the leading cause of morbidity and mortality in the Western world, and the primary cause of myocardial infarction, stroke, and ischemia. The biology of vascular disease is complex and still poorly understood in terms of causes and consequences. Vascular function is determined by structural and functional properties of the arterial vascular wall. Arterial stiffness, that is a pathological alteration of the vascular wall, ultimately results in target-organ damage and increased mortality… Show more

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Cited by 136 publications
(111 citation statements)
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“…Thus, a possible explanation could be that increased endostatin mirrors a systemic elevated angiogenic activity, reflecting increased neovascularization induced by vascular, myocardial, or renal ischemia, similar as the role suggested for vascular endothelial growth factor. 4,13,14,[36][37][38] Endostatin has also been shown to exert acute reductions in blood pressure via a release of NO, 39 and individuals with Down Syndrome have significantly higher circulating levels of endostatin and exhibit lower blood pressure compared with control subjects. 40,41 This may indicate that endostatin, per se, may exert a blood pressure lowering effect.…”
Section: Discussionmentioning
confidence: 99%
See 1 more Smart Citation
“…Thus, a possible explanation could be that increased endostatin mirrors a systemic elevated angiogenic activity, reflecting increased neovascularization induced by vascular, myocardial, or renal ischemia, similar as the role suggested for vascular endothelial growth factor. 4,13,14,[36][37][38] Endostatin has also been shown to exert acute reductions in blood pressure via a release of NO, 39 and individuals with Down Syndrome have significantly higher circulating levels of endostatin and exhibit lower blood pressure compared with control subjects. 40,41 This may indicate that endostatin, per se, may exert a blood pressure lowering effect.…”
Section: Discussionmentioning
confidence: 99%
“…4,13,14 Meanwhile, extracellular matrix proteinases also increase in those tissues. 4,15,16 Thus, endostatin, a cleaved product of collagen XVIII, could be an indicator of adverse extracellular remodeling in hypertension.…”
mentioning
confidence: 99%
“…The mechanisms involved include fibrosis, hyperplasia, and hypertrophy of vascular smooth muscle cells, loss of contractility of vascular smooth muscle cells, deposition of collagen, fragmentation of the elastic lamina, endothelial dysfunction, and arterial calcification. 5 Collectively, these vascular changes alter the pressure waveform of the aorta, which is composed of a forward traveling wave generated by cardiac contraction and a backwards traveling wave generated by reflection from peripheral arteries. The latter is generated at vascular bifurcations and at sites where elastic conduit arteries convert into muscular resistance arteries.…”
Section: Pathophysiology Of Bp Regulation In the Oldest Oldmentioning
confidence: 99%
“…Namely, Russians may develop atherosclerosis-related conditions at a younger age than Japanese subjects, which is supported by the WHO data for CVD 14) . tion of oxidative stress and inflammation 7,18,29) . The NOS3 gene is responsible for the endothelial NOS production 17) , and NOS3 -786T C has been reported to be associated with CVD 16) .…”
Section: Discussionmentioning
confidence: 99%
“…Atherogenesis is the basic cause underlying the development of CVD 5) . Arterial stiffness and endothelial dysfunction are associated with the progression of atherosclerosis, including vascular plaque formation, along with arterial media remodeling 6,7) , and these are predictive of damage to target organs such as Russian males was odd, one Japanese subject was allocated to one Russian subject in one case. Both Russian and Japanese subjects were volunteers recruited from local medical students.…”
Section: Introductionmentioning
confidence: 99%