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Int J Biol Sci. 2018 Sep 7;14(12):1645-1657. doi: 10.7150/ijbs.28103. eCollection 2018.

Cardiac fibrosis: new insights into the pathogenesis.

Ma ZG1,2,3, Yuan YP1,2,3, Wu HM1,2,3, Zhang X1,2,3, Tang QZ1,2,3.

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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.


Cardiac fibroblast; Cardiac fibrosis; Smad; TGF-β

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Competing Interests: The authors have declared that no competing interest exists.

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