کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8475155 | 1550444 | 2013 | 8 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Redox-dependent regulation of the Na+-K+ pump: New twists to an old target for treatment of heart failure
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کلمات کلیدی
pKaSGCPKGPKCGRX1intracellular Na+ concentrationPP2AACEGSHNa+–K+ pumpcAMP - cAMPONOO− - ONOO-[Na+]i - [Na +] Iangiotensin converting enzyme - آنزیم تبدیل آنژیوتانسینAngiotensin II - آنژیوتانسین دوNADPH oxidase - اکسیداز NADPH Soluble guanylyl cyclase - حلال گویینیل سیکلاسAng II - دومRedox regulation - مقررات Redoxheart failure - نارسایی قلبیNitric oxide - نیتریک اکسیدnicotinamide adenine dinucleotide phosphate-oxidase - نیکوتین آمید آدنین دیونوکلئوتید فسفات اکسیدازprotein phosphatase 2A - پروتئین فسفاتاز 2Aprotein kinase A - پروتئین کیناز Aprotein kinase G - پروتئین کیناز GProtein kinase C - پروتئین کیناز سیPeroxynitrite - پروکسی نیتریتGlutathione - گلوتاتیونGlutaredoxin 1 - گلوتاراکسین 1adrenergic receptor - گیرنده آدرنرژیک
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
بیولوژی سلول
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: Redox-dependent regulation of the Na+-K+ pump: New twists to an old target for treatment of heart failure Redox-dependent regulation of the Na+-K+ pump: New twists to an old target for treatment of heart failure](/preview/png/8475155.png)
چکیده انگلیسی
By the time it was appreciated that the positive inotropic effect of cardiac glycosides is due to inhibition of the membrane Na+-K+ pump, glycosides had been used for treatment of heart failure on an empiric basis for ~Â 200Â years. The subsequent documentation of their lack of clinical efficacy and possible harmful effect largely coincided with the discovery that a raised Na+ concentration in cardiac myocytes plays an important role in the electromechanical phenotype of heart failure syndromes. Consistent with this, efficacious pharmacological treatments for heart failure have been found to stimulate the Na+-K+ pump, effectively the only export route for intracellular Na+ in the heart failure. A paradigm has emerged that implicates pump inhibition in the raised Na+ levels in heart failure. It invokes protein kinase-dependent activation of nicotinamide adenine dinucleotide phosphate oxidase (NADPH oxidase) and glutathionylation, a reversible oxidative modification, of the Na+-K+ pump molecular complex that inhibits its activity. Since treatments of proven efficacy reverse the oxidative Na+-K+ pump inhibition, the pump retains its status as a key pharmacological target in heart failure. Its role as a target is well integrated with the paradigms of neurohormonal abnormalities, raised myocardial oxidative stress and energy deficiency implicated in the pathophysiology of the failing heart. We propose that targeting oxidative inhibition of the pump is useful for the exploration of future treatment strategies. This article is part of a Special Issue entitled “Na+Â Regulation in Cardiac Myocytes”.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Journal of Molecular and Cellular Cardiology - Volume 61, August 2013, Pages 94-101
Journal: Journal of Molecular and Cellular Cardiology - Volume 61, August 2013, Pages 94-101
نویسندگان
Chia-Chi Liu, Natasha A.S. Fry, Elisha J. Hamilton, Karin K.M. Chia, Alvaro Garcia, Keyvan Karimi Galougahi, Gemma A. Figtree, Ronald J. Clarke, Henning Bundgaard, Helge H. Rasmussen,