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Review
. 2017 Apr 24:8:238.
doi: 10.3389/fphys.2017.00238. eCollection 2017.

Current Understanding of the Pathophysiology of Myocardial Fibrosis and Its Quantitative Assessment in Heart Failure

Tong Liu  1 , Deli Song  1 , Jianzeng Dong  1 , Pinghui Zhu  2 , Jie Liu  3   4 , Wei Liu  1 , Xiaohai Ma  5 , Lei Zhao  5 , Shukuan Ling  6
Affiliations
Review

Current Understanding of the Pathophysiology of Myocardial Fibrosis and Its Quantitative Assessment in Heart Failure

Tong Liu et al. Front Physiol. .

Abstract

Myocardial fibrosis is an important part of cardiac remodeling that leads to heart failure and death. Myocardial fibrosis results from increased myofibroblast activity and excessive extracellular matrix deposition. Various cells and molecules are involved in this process, providing targets for potential drug therapies. Currently, the main detection methods of myocardial fibrosis rely on serum markers, cardiac magnetic resonance imaging, and endomyocardial biopsy. This review summarizes our current knowledge regarding the pathophysiology, quantitative assessment, and novel therapeutic strategies of myocardial fibrosis.

Keywords: biomarkers; extracelluar matrix; heart failure; late gadolinium enhancement; micro RNAs (miRNAs); mycardial fibrosis.

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Figures

Figure 1
Figure 1
Origins and activation of myofibroblasts. Myofibroblasts can be activated in different situations such as myocardial injury, pressure overload, and genetic abnormalities. Myofibroblasts may be derived from resident fibroblasts, bone marrow-derived fibroblasts, epithelial-to-mesenchymal transition, and endothelial-to-mesenchymal transition (EndMT). The contribution of different origins may be variable in different etiologies.
Figure 2
Figure 2
Inflammatory response in myocardial fibrosis.
See this image and copyright information in PMC

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