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Function and fate of myofibroblasts after myocardial infarction

Neil A Turner* and Karen E Porter

Author Affiliations

Division of Cardiovascular and Diabetes Research, and Multidisciplinary Cardiovascular Research Centre, School of Medicine, University of Leeds, Leeds LS2 9JT, UK

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Fibrogenesis & Tissue Repair 2013, 6:5  doi:10.1186/1755-1536-6-5

Published: 1 March 2013


The importance of cardiac fibroblasts in the regulation of myocardial remodelling following myocardial infarction (MI) is becoming increasingly recognised. Studies over the last few decades have reinforced the concept that cardiac fibroblasts are much more than simple homeostatic regulators of extracellular matrix turnover, but are integrally involved in all aspects of the repair and remodelling of the heart that occurs following MI. The plasticity of fibroblasts is due in part to their ability to undergo differentiation into myofibroblasts. Myofibroblasts are specialised cells that possess a more contractile and synthetic phenotype than fibroblasts, enabling them to effectively repair and remodel the cardiac interstitium to manage the local devastation caused by MI. However, in addition to their key role in cardiac restoration and healing, persistence of myofibroblast activation can drive pathological fibrosis, resulting in arrhythmias, myocardial stiffness and progression to heart failure. The aim of this review is to give an appreciation of both the beneficial and detrimental roles of the myofibroblast in the remodelling heart, to describe some of the major regulatory mechanisms controlling myofibroblast differentiation including recent advances in the microRNA field, and to consider how this cell type could be exploited therapeutically.

Myofibroblasts; Heart; Myocardial infarction; Remodelling; Fibrosis