کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
5828779 1558980 2013 7 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
ReviewMechanisms of epoxyeicosatrienoic acids to improve cardiac remodeling in chronic renal failure disease
ترجمه فارسی عنوان
بررسی مکانیسم اسیدهای اپوکسی ایزواتروئیدیک برای بهبود ترمیم قلب در بیماری های مزمن کلیوی
کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری علم عصب شناسی علوم اعصاب سلولی و مولکولی
چکیده انگلیسی

Both clinical and basic science studies have demonstrated that cardiac remodeling in patients with chronic renal failure (CRF) is very common. It is a key feature during the course of heart failure and an important risk factor for subsequent cardiac mortality. Traditional drugs or therapies rarely have effects on cardiac regression of CRF and cardiovascular events are still the first cause of death. Epoxyeicosatrienoic acids (EETs) are the products of arachidonic acids metabolized by cytochrome P450 epoxygenases. It has been found that EETs have important biological effects including anti-hypertension and anti-inflammation. Recent data suggest that EETs are involved in regulating cardiomyocyte injury, renal dysfunction, chronic kidney disease (CKD)-related risk factors and signaling pathways, all of which play key roles in cardiac remodeling induced by CRF. This review analyzes the literature to identify the possible mechanisms for EETs to improve cardiac remodeling induced by CRF and indicates the therapeutic potential of EETs in it.

Cardiomyocyte injury, renal dysfunction, chronic kidney disease (CKD)-related risk factors and signaling pathways are all involved in the process of cardiac remodeling induced by chronic renal failure (CRF). EETs upregulation may be a potential therapy to improve CRF-induced cardiac remodeling by regulating cardiomyocyte injury, renal function, CKD-related risk factors and signaling pathways.178

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: European Journal of Pharmacology - Volume 701, Issues 1–3, 15 February 2013, Pages 33-39
نویسندگان
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