کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5501884 | 1534934 | 2017 | 29 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Vascular remodeling: A redox-modulated mechanism of vessel caliber regulation
ترجمه فارسی عنوان
تغییرات عروقی: یک مکانیزم ردوکس مدولاسیون تنظیم کالیبراسیون کشتی
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کلمات کلیدی
AMPKERp57Col3a1CuZnSODeNOSECMCaMKIIAAAAMP-activated protein kinase - AMP-پروتئین کیناز فعال شده استecSOD - ecsodAbdominal aortic aneurysm - آنوریسمی آئورت شکمیApoe - آپوapolipoprotein E - آپولیپوپروتئین EElectron paramagnetic resonance - تشدید پارامغناطیس الکترونEPR - تشدید پارامغناطیس الکترونendothelial nitric oxide synthase - سنتاز اکسید نیتریک اندوتلیالendoplasmic reticulum - شبکه آندوپلاسمی Extracellular matrix - ماتریکس خارج سلولیcalcium/calmodulin-dependent protein kinase II - پروتئین کیناز II وابسته به کلسیم / کالودولین
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
سالمندی
چکیده انگلیسی
Vascular remodeling, i.e. whole-vessel structural reshaping, determines lumen caliber in (patho)physiology. Here we review mechanisms underlying vessel remodeling, with emphasis in redox regulation. First, we discuss confusing terminology and focus on strictu sensu remodeling. Second, we propose a mechanobiological remodeling paradigm based on the concept of tensional homeostasis as a setpoint regulator. We first focus on shear-mediated models as prototypes of remodeling closely dominated by highly redox-sensitive endothelial function. More detailed discussions focus on mechanosensors, integrins, extracellular matrix, cytoskeleton and inflammatory pathways as potential of mechanisms potentially coupling tensional homeostasis to redox regulation. Further discussion of remodeling associated with atherosclerosis and injury repair highlights important aspects of redox vascular responses. While neointima formation has not shown consistent responsiveness to antioxidants, vessel remodeling has been more clearly responsive, indicating that despite the multilevel redox signaling pathways, there is a coordinated response of the whole vessel. Among mechanisms that may orchestrate redox pathways, we discuss roles of superoxide dismutase activity and extracellular protein disulfide isomerase. We then discuss redox modulation of aneurysms, a special case of expansive remodeling. We propose that the redox modulation of vascular remodeling may reflect (1) remodeling pathophysiology is dominated by a particularly redox-sensitive cell type, e.g., endothelial cells (2) redox pathways are temporospatially coordinated at an organ level across distinct cellular and acellular structures or (3) the tensional homeostasis setpoint is closely connected to redox signaling. The mechanobiological/redox model discussed here can be a basis for improved understanding of remodeling and helps clarifying mechanisms underlying prevalent hard-to-treat diseases.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Free Radical Biology and Medicine - Volume 109, August 2017, Pages 11-21
Journal: Free Radical Biology and Medicine - Volume 109, August 2017, Pages 11-21
نویسندگان
Leonardo Y. Tanaka, Francisco R.M. Laurindo,