S100A1: A Novel and Essential Molecular Component for Postischemic Angiogenesis
نویسندگان
چکیده
منابع مشابه
S100A1: A novel and essential molecular component for postischemic angiogenesis.
C ritical limb ischemia is associated with significant morbidity and mortality. Revascularization is not always feasible or successful. Consequently, in a worryingly high percentage of patients, amputation is the only option. It is hoped that a wider understanding of the molecular mechanisms underpinning limb ischemia can help develop new and truly revolutionary therapeutic strategies. In this ...
متن کاملS100A1 deficiency impairs postischemic angiogenesis via compromised proangiogenic endothelial cell function and nitric oxide synthase regulation.
RATIONALE Mice lacking the EF-hand Ca2+ sensor S100A1 display endothelial dysfunction because of distorted Ca2+ -activated nitric oxide (NO) generation. OBJECTIVE To determine the pathophysiological role of S100A1 in endothelial cell (EC) function in experimental ischemic revascularization. METHODS AND RESULTS Patients with chronic critical limb ischemia showed almost complete loss of S100A...
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this study intends to investigate samuel beckett’s waiting for godot and endgame under the lacanian psychoanalysis. it begins by explaining the most important concepts of lacanian psychoanalysis. the beckettian characters are studied regarding their state of unconscious, and not the state of consciousness as is common in most beckett studies. according to lacan, language plays the sole role in ...
S100A1: a novel inotropic regulator of cardiac performance. Transition from molecular physiology to pathophysiological relevance.
Here we review the considerable body of evidence that has accumulated to support the notion of S100A1, a cardiac-specific Ca(2+)-sensor protein of the EF-hand type, as a physiological regulator of excitation-contraction coupling and inotropic reserve mechanisms in the mammalian heart. In particular, molecular mechanisms will be discussed conveying the Ca(2+)-dependent inotropic actions of S100A...
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Background—Excessive formation of reactive oxygen species contributes to tissue injury and functional deterioration after myocardial ischemia/reperfusion. Especially, mitochondrial reactive oxygen species are capable of opening the mitochondrial permeability transition pore, a harmful event in cardiac ischemia/reperfusion. Thioredoxins are key players in the cardiac defense against oxidative st...
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ژورنال
عنوان ژورنال: Circulation Research
سال: 2013
ISSN: 0009-7330,1524-4571
DOI: 10.1161/circresaha.112.281022