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Int J Biol Sci 2018; 14(12):1645-1657. doi:10.7150/ijbs.28103


Cardiac fibrosis: new insights into the pathogenesis

Zhen-Guo Ma, Yu-Pei Yuan, Hai-Ming Wu, Xin Zhang, Qi-Zhu Tang

Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan 430060, RP China
Cardiovascular Research Institute of Wuhan University, Wuhan 430060, RP China
Hubei Key Laboratory of Cardiology, Wuhan 430060, RP China


Cardiac fibrosis is defined as the imbalance of extracellular matrix (ECM) production and degradation, thus contributing to cardiac dysfunction in many cardiac pathophysiologic conditions. This review discusses specific markers and origin of cardiac fibroblasts (CFs), and the underlying mechanism involved in the development of cardiac fibrosis. Currently, there are no CFs-specific molecular markers. Most studies use co-labelling with panels of antibodies that can recognize CFs. Origin of fibroblasts is heterogeneous. After fibrotic stimuli, the levels of myocardial pro-fibrotic growth factors and cytokines are increased. These pro-fibrotic growth factors and cytokines bind to its receptors and then trigger the activation of signaling pathway and transcriptional factors via Smad-dependent or Smad independent-manners. These fibrosis-related transcriptional factors regulate gene expression that are involved in the fibrosis to amplify the fibrotic response. Understanding the mechanisms responsible for initiation, progression, and amplification of cardiac fibrosis are of great clinical significance to find drugs that can prevent the progression of cardiac fibrosis.

Keywords: Cardiac fibrosis, Cardiac fibroblast, TGF-β, Smad

This is an open access article distributed under the terms of the Creative Commons Attribution (CC BY-NC) license ( See for full terms and conditions.
How to cite this article:
Ma ZG, Yuan YP, Wu HM, Zhang X, Tang QZ. Cardiac fibrosis: new insights into the pathogenesis. Int J Biol Sci 2018; 14(12):1645-1657. doi:10.7150/ijbs.28103. Available from