کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5843961 | 1560958 | 2015 | 34 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Histone deacetylases as therapeutic targets - From cancer to cardiac disease
ترجمه فارسی عنوان
هیستون دیازتیلاس به عنوان اهداف درمانی - از سرطان به بیماری قلبی
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کلمات کلیدی
MEF2TSAHistone deacetylases inhibitorsHDACDOCAVPAHDACiSAHATrichostatin A - تریکوستاتین Adeoxycorticosterone acetate - دئوسکوکورتیکوسترون استاتmyocyte enhancer factor-2 - عامل افزایش دهنده myocyte-2histone deacetylase inhibitor - مهار کننده هیستون داسیدلازheart failure - نارسایی قلبیhistone deacetylases - هیستون deacetylaseshistone acetyltransferases - هیستون استیل ترانسفرازhistone deacetylase - هیستون داستیلازHypertrophy - هیپرتروفی یا پُرسازیValproic acid - والپروات و والپروات سدیم یا والپروئیک اسیدHAT - کلاه
موضوعات مرتبط
علوم پزشکی و سلامت
داروسازی، سم شناسی و علوم دارویی
داروشناسی
چکیده انگلیسی
Heart failure is a major public health problem in western society. Recently, agents that inhibit histone deacetylase (HDAC) enzymes were developed and approved by the FDA as anticancer agents. This breakthrough has provided the motivation to develop more potent and more selective HDAC inhibitors and to target other pathologic conditions with these drugs. Here we review experimental evidence showing that these drugs may be beneficial in preventing cardiac hypertrophy and heart failure. Several lines of evidence show that inhibitors of Class I HDACs can blunt cardiac hypertrophy and preserve cardiac function in several small animal models. In contrast, Class IIa HDACs appear to be suppressors of hypertrophy, though experimental data with small molecule blockers of this class is largely lacking. The effects of HDAC inhibition in cardiac diseases, the cell population in the heart that is targeted by HDAC blockers, as well as the relative roles of specific HDACs are still under intense investigation.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Pharmacology & Therapeutics - Volume 147, March 2015, Pages 55-62
Journal: Pharmacology & Therapeutics - Volume 147, March 2015, Pages 55-62
نویسندگان
Alon Abend, Izhak Kehat,