کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10883572 | 1078459 | 2013 | 5 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
RASSF1A: A potential novel therapeutic target against cardiac hypertrophy
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کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
بیوفیزیک
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چکیده انگلیسی
Cardiac hypertrophy is a key risk factor for chronic heart failure. Current treatments predominantly focus on both reducing the peripheral vascular resistance and activating nerve-humoral system. However, these efforts can't reverse cardiac hypertrophy fundamentally. Ras association domain family 1 isoform A (RASSF1A) is a regulatory tumor suppressor whose inactivation by inappropriate promoter methylation has been implicated in the development of many human cancers. Recently, there have been a number of studies investigating the roles of RASSF1A in the pathophysiology of cardiac hypertrophy. In this review, we focus on the present progresses of cardiac RASSF1A under physiological and pathological conditions, trying to systematically elucidate how the RASSF1A-mediated signal pathways contribute to the maintenance of normal cardiac myocyte structure and function and lead to the regression of pathological cardiac hypertrophy. These pathways exert multiple functions such as regulating cardiac contractility, physiologically increasing stability of microtubule, preventing cardiac dysfunction, attenuating interstitial fibrosis and mediating cell apoptosis. These specific roles are highly relevant with cardiac hemodynamics and therapeutic strategies, indicating RASSF1A may have the potential to reverse pathological cardiac hypertrophy thus prevent heart failure fundamentally.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Progress in Biophysics and Molecular Biology - Volume 113, Issue 2, November 2013, Pages 284-288
Journal: Progress in Biophysics and Molecular Biology - Volume 113, Issue 2, November 2013, Pages 284-288
نویسندگان
Chenyang Duan, Mengying Liu, Jiqiang Zhang, Ruiyan Ma,