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miR-29a attenuates cardiac hypertrophy through inhibition of PPARδ expression.

Zhang, Si; Yin, Zhongnan; Dai, Fei-Fei; Wang, Hao; Zhou, Meng-Jiao; Yang, Ming-Hui; Zhang, Shu-Feng; Fu, Zhi-Feng; Mei, Ying-Wu; Zang, Ming-Xi; Xue, Lixiang.
J Cell Physiol; 234(8): 13252-13262, 2019 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-30580435
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.
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