Aab Cardiovascular Research Institute, Department of Medicine, School of Medicine and Dentistry, University of Rochester, 601 Elmwood Avenue, Box CVRI, Rochester, NY 14642, USA.
J Cardiovasc Transl Res. 2012 Dec;5(6):794-804. doi: 10.1007/s12265-012-9397-0. Epub 2012 Aug 17.
Cardiac fibroblasts are responsible for necrotic tissue replacement and scar formation after myocardial infarction (MI) and contribute to remodeling in response to pathological stimuli. This response to insult or injury is largely due to the phenotypic plasticity of fibroblasts. When fibroblasts encounter environmental disturbances, whether biomechanical or humoral, they often transform into smooth muscle-like, contractile cells called "myofibroblasts." The signals that control myofibroblast differentiation include the transforming growth factor (TGF)-β1-Smad pathway and Rho GTPase-dependent actin polymerization. Recent evidence implicates serum response factor (SRF) and the myocardin-related transcription factors (MRTFs) as key mediators of the contractile gene program in response to TGF-β1 or RhoA signaling. This review highlights the function of myofibroblasts in cardiac remodeling and the role of the actin-MRTF-SRF signaling axis in regulating this process.
心肌成纤维细胞负责心肌梗死（MI）后坏死组织的替代和瘢痕形成，并对病理性刺激做出重塑反应。这种对损伤或刺激的反应主要归因于成纤维细胞的表型可塑性。当成纤维细胞遇到环境干扰，无论是力学的还是体液的，它们通常会转化为称为“肌成纤维细胞”的平滑肌样收缩细胞。控制肌成纤维细胞分化的信号包括转化生长因子（TGF）-β1-Smad 通路和 Rho GTP 酶依赖性肌动蛋白聚合。最近的证据表明血清反应因子（SRF）和肌球蛋白相关转录因子（MRTFs）是 TGF-β1 或 RhoA 信号转导中收缩基因程序的关键介质。这篇综述强调了肌成纤维细胞在心脏重塑中的作用以及肌动蛋白-MRTF-SRF 信号轴在调节这一过程中的作用。
