Preprint Review Version 1 Preserved in Portico This version is not peer-reviewed

Cardiac Myofibroblast and Fibrosis

Version 1 : Received: 18 May 2021 / Approved: 19 May 2021 / Online: 19 May 2021 (07:55:59 CEST)

A peer-reviewed article of this Preprint also exists.

Kurose, H. Cardiac Fibrosis and Fibroblasts. Cells 2021, 10, 1716. Kurose, H. Cardiac Fibrosis and Fibroblasts. Cells 2021, 10, 1716.


Fibroblasts are differentiated to myofibroblasts and produce collagen and other extracellular matrix when the heart is exposed to stresses. Myocardial infarction and pressure overload-induced hypertrophy are major stresses to induce differentiation of fibroblasts. Since collagen can compensate the missing tissue due to injury, appropriate production of collagen is beneficial for the injured heart against rupture. However, excessive deposition of collagen is called fibrosis and causes cardiac dysfunction. After fibroblasts are differentiated to myofibroblasts, myofibroblasts can further change their phenotypes. In addition, myofibroblasts are found to have a new function other than collagen production. Myofibroblasts have macrophage-like functions that engulf dead cells and secrete anti-inflammatory cytokines. So far, research on fibroblasts has been delayed due to the lack of available markers for selective isolation of fibroblasts. In recent years, it has become possible to genetically label fibroblasts, sequence the cells at single cell levels, and manipulate function or the number of cells. Based on new technologies, the origin of fibroblasts and myofibroblasts, time-dependent changes of fibroblast states after injury, and heterogeneity have been demonstrated. Here, I will introduce recent advances in fibroblasts and myofibroblasts.


myofibroblasts; fibrosis; heart failure


Medicine and Pharmacology, Immunology and Allergy

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