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miR‐29a attenuates cardiac hypertrophy through inhibition of PPARδ expression
Author(s) -
Zhang Si,
Yin Zhongnan,
Dai FeiFei,
Wang Hao,
Zhou MengJiao,
Yang MingHui,
Zhang ShuFeng,
Fu ZhiFeng,
Mei YingWu,
Zang MingXi,
Xue Lixiang
Publication year - 2019
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.27997
Subject(s) - cardiac hypertrophy , peroxisome proliferator activated receptor , muscle hypertrophy , microbiology and biotechnology , medicine , chemistry , endocrinology , biology , receptor
Although cardiac hypertrophy is widely recognized as a risk factor that leads to cardiac dysfunction and, ultimately, heart failure, the complex mechanisms underlying cardiac hypertrophy remain incompletely characterized. The nuclear receptor peroxisome proliferator‐activated receptor δ (PPARδ) is involved in the regulation of cardiac lipid metabolism. Here, we describe a novel PPARδ‐dependent molecular cascade involving microRNA‐29a (miR‐29a) and atrial natriuretic factor (ANF), which is reactivated in cardiac hypertrophy. In addition, we identify a novel role of miR‐29a, in which it has a cardioprotective function in isoproterenol hydrochloride‐induced cardiac hypertrophy by targeting PPARδ and downregulating ANF. Finally, we provide evidence that miR‐29a reduces the isoproterenol hydrochloride‐induced cardiac hypertrophy response, thereby underlining the potential clinical relevance of miR‐29a in which it may serve as a potent therapeutic target for heart hypertrophy treatment.