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

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

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

Author: Dan XIAO ¹ ; Yue ZHANG ¹ ; Rui WANG ¹ ; Yujie FU ¹ ; Tong ZHOU ² ; Hongtao DIAO ¹ ; Zhixia WANG ¹ ; Yuan LIN ¹ ; Zhange LI ¹ ; Lin WEN ¹ ; Xujuan KANG ¹ ; Philipp KOPYLOV ³ ; Dmitri SHCHEKOCHIKHIN ³ ; Yong ZHANG ¹ ; Baofeng YANG ¹
Author Information

1. Department of Pharmacology (State-Province Key Laboratories of Biomedicine-Pharmaceutics of China, Key Laboratory of Cardiovascular Research, Ministry of Education), Harbin Medical University, Harbin 150081, China.
2. Department of Pharmacy, The First Affiliated Hospital of Harbin Medical University, Harbin 150081, China.
3. Department of Preventive and Emergency Cardiology, Sechenov First Moscow State Medical University, Moscow 119991, Russian Federation.
Publication Type:Journal Article
Keywords: Angiotensin II; Cardiac fibroblast; Cardiac fibrosis; Emodin; MTA3; Mouse
From: Acta Pharmaceutica Sinica B 2019;9(4):724-733
CountryChina
Language:English
Abstract: 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 fibrosis upregulating MTA3 and highlight the regulatory role of MTA3 in the development of cardiac fibrosis.