Oncotarget

Reviews:

Transforming growth factor β: A potential biomarker and therapeutic target of ventricular remodeling

Yuan Ma, Hai Zou, Xing-Xing Zhu, Jie Pang, Qiang Xu, Qin-Yang Jin, Ya-Hui Ding, Bing Zhou and Dong-Sheng Huang _

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Oncotarget. 2017; 8:53780-53790. https://doi.org/10.18632/oncotarget.17255

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Abstract

Yuan Ma1,5,*, Hai Zou1,5,*, Xing-Xing Zhu2,5,*, Jie Pang1,5, Qiang Xu1,5, Qin-Yang Jin1,5, Ya-Hui Ding1,5, Bing Zhou3,5 and Dong-Sheng Huang4,5

1Department of Cardiology, Zhejiang Provincial People's Hospital, Hangzhou, China

2Department of Nephrology, Zhejiang Provincial People's Hospital, Hangzhou, China

3Department of Cardiac Surgery, Zhejiang Provincial People's Hospital, Hangzhou, China

4Department of Hepatobiliary Surgery, Zhejiang Provincial People's Hospital, Hangzhou, China

5People’s Hospital of Hangzhou Medical College, Hangzhou, China

*Co-first authors

Correspondence to:

Bing Zhou, email: zhoubing@zjheart.com

Ya-Hui Ding, email: dyh@zjheart.com

Hai Zou, email: haire1993@163.com

Dong-Sheng Huang, email: dshuang@zjheart.com

Keywords: transforming growth factor β, myocardial fibrosis, ventricular remodeling, mechanism, targets

Received: February 06, 2017     Accepted: April 11, 2017     Published: April 19, 2017

ABSTRACT

Transforming growth factor β (TGF-β) is a multifunctional cytokine that is synthesized by many types of cells and regulates the cell cycle. Increasing evidence has led to TGF-β receiving increased and deserved attention in recent years because it may play a potentially novel and critical role in the development and progression of myocardial fibrosis and the subsequent progress of ventricular remodeling (VR). Numerous studies have highlighted a crucial role of TGF-β in VR and suggest potential therapeutic targets of the TGF-β signaling pathways for VR. Changes in TGF-β activity may elicit anti-VR activity and may serve as a novel therapeutic target for VR therapy. This review we discusses the smad-dependent signaling pathway, such as TGF-β/Smads, TGF-β/Sirtuins, TGF-β/BMP, TGF-β/miRNAs, TGF-β/MAPK, and Smad-independent signaling pathway of TGF-β, such as TGF-β/PI3K/Akt, TGF-β/Rho/ROCK,TGF-β/Wnt/β-catenin in the cardiac fibrosis and subsequent progression of VR. Furthermore, agonists and antagonists of TGF-β as potential therapeutic targets in VR are also described.


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