Turner Neil A, Porter Karen E
Division of Cardiovascular and Diabetes Research, and Multidisciplinary Cardiovascular Research Centre, School of Medicine, University of Leeds, Leeds LS2 9JT, UK.
Fibrogenesis Tissue Repair. 2013 Mar 1;6(1):5. doi: 10.1186/1755-1536-6-5.
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.
心脏成纤维细胞在心肌梗死（MI）后心肌重塑调节中的重要性日益受到认可。过去几十年的研究强化了这样一个概念，即心脏成纤维细胞远不止是细胞外基质周转的简单稳态调节因子，而是全面参与MI后心脏修复和重塑的各个方面。成纤维细胞的可塑性部分归因于它们分化为肌成纤维细胞的能力。肌成纤维细胞是一种特殊的细胞，与成纤维细胞相比，具有更强的收缩和合成表型，使其能够有效地修复和重塑心脏间质，以应对MI造成的局部破坏。然而，除了在心脏恢复和愈合中的关键作用外，肌成纤维细胞激活的持续存在可导致病理性纤维化，进而引发心律失常、心肌僵硬并进展为心力衰竭。本综述的目的是认识肌成纤维细胞在重塑心脏中的有益和有害作用，描述一些控制肌成纤维细胞分化的主要调节机制，包括微小RNA领域的最新进展，并探讨如何从治疗上利用这种细胞类型。
