Article Publish Status: FREE
Abstract Title:

Emodin alleviates cardiac fibrosis by suppressing activation of cardiac fibroblastsupregulating metastasis associated protein 3.

Abstract Source:

Acta Pharm Sin B. 2019 Jul ;9(4):724-733. Epub 2019 Apr 22. PMID: 31384533

Abstract Author(s):

Dan Xiao, Yue Zhang, Rui Wang, Yujie Fu, Tong Zhou, Hongtao Diao, Zhixia Wang, Yuan Lin, Zhange Li, Lin Wen, Xujuan Kang, Philipp Kopylov, Dmitri Shchekochikhin, Yong Zhang, Baofeng Yang

Article Affiliation:

Dan Xiao


Excess activation of cardiac fibroblasts inevitably induces cardiac fibrosis. Emodin has been used as a natural medicine against several chronic diseases. The objective of this study is to determine the effects of emodin on cardiac fibrosis and the underlying molecular mechanisms. Intragastric administration of emodin markedly decreased left ventricular wall thickness in a mouse model of pathological cardiac hypertrophy with excess fibrosis induced by transaortic constriction (TAC) and suppressed activation of cardiac fibroblasts induced by angiotensin II (AngII). Emodin upregulated expression of metastasis associated protein 3 (MTA3) and restored the MTA3 expression in the setting of cardiac fibrosis. Moreover, overexpression of MTA3 promoted cardiac fibrosis; in contrast, silence of MTA3 abrogated the inhibitory effect of emodin on fibroblast activation. Our findings unraveled the potential of emodin to alleviate cardiac fibrosisupregulating MTA3 and highlight the regulatory role of MTA3 in the development of cardiac fibrosis.

Study Type : Animal Study

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