Current Pathobiology Reports

, Volume 5, Issue 2, pp 145–152 | Cite as

Mechanisms of Fibroblast Activation in the Remodeling Myocardium

Activated Myofibroblasts and Fibrosis in Various Organs (T Kisseleva and Y Liu, Section Editors)
Part of the following topical collections:
  1. Topical Collection on Activated Myofibroblasts and Fibrosis in Various Organs

Abstract

Purpose of Review

Activated fibroblasts are critically implicated in repair and remodeling of the injured heart. This manuscript discusses recent progress in the cell biology of fibroblasts in the infarcted and remodeling myocardium, highlighting advances in understanding the origin, function, and mechanisms of activation of these cells.

Recent Findings

Following myocardial injury, fibroblasts undergo activation and myofibroblast transdifferentiation. Recently published studies have suggested that most activated myofibroblasts in the infarcted and pressure-overloaded hearts are derived from resident fibroblast populations. In the healing infarct, fibroblasts undergo dynamic phenotypic alterations in response to changes in the cytokine milieu and in the composition of the extracellular matrix. Fibroblasts do not simply serve as matrix-producing cells, but may also regulate inflammation, modulate cardiomyocyte survival and function, mediate angiogenesis, and contribute to phagocytosis of dead cells.

Summary

In the injured myocardium, fibroblasts are derived predominantly from resident populations and serve a wide range of functions.

Keywords

Fibroblast Myofibroblast Myocardial infarction Cardiac remodeling Cytokine 

Notes

Compliance with Ethical Standards

Conflict of Interest

Arti Shinde and Nikolaos Frangogiannis declare that they have no conflicts of interest.

Human and Animal Rights and Informed Consent

This article does not contain any studies with human or animal subjects performed by any of the authors.

Sources of Funding

Supported by grants from the National Institutes of Health (R01 HL76246 and R01 HL85440 to N.G.F.), the Department of Defense (PR151134 and PR151029 to N.G.F.) and a post-doctoral award by the American Heart Association Founders’ affiliate (to A.V.S.).

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Copyright information

© Springer Science+Business Media New York 2017

Authors and Affiliations

  1. 1.The Wilf Family Cardiovascular Research Institute, Department of Medicine, Division of CardiologyAlbert Einstein College of MedicineBronxUSA
  2. 2.Division of Cardiology, the Wilf Cardiovascular Research InstituteAlbert Einstein College of MedicineBronxUSA

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