Department of Cellular and Integrative Physiology, Center for Heart and Vascular Research, University of Nebraska Medical Center, 985850 Nebraska Medical Center Omaha, NE 68198-5850, USA; Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson, MS, 39216, USA; Research Service, Nebraska-Western Iowa Health Care System, Omaha, NE 68198, USA.
Department of Cellular and Integrative Physiology, Center for Heart and Vascular Research, University of Nebraska Medical Center, 985850 Nebraska Medical Center Omaha, NE 68198-5850, USA; Research Service, Nebraska-Western Iowa Health Care System, Omaha, NE 68198, USA.
Matrix Biol. 2020 Sep;91-92:109-116. doi: 10.1016/j.matbio.2020.03.010. Epub 2020 May 21.
Cardiac wound healing after myocardial infarction (MI) evolves from pro-inflammatory to anti-inflammatory to reparative responses, and the cardiac fibroblast is a central player during the entire transition. The fibroblast mirrors changes seen in the left ventricle infarct by undergoing a continuum of polarization phenotypes that follow pro-inflammatory, anti-inflammatory, and pro-scar producing profiles. The development of each phenotype transition is contingent upon the MI environment into which the fibroblast enters. In this mini-review, we summarize our current knowledge regarding cardiac fibroblast activation during MI and highlight key areas where gaps remain.
心肌梗死后的心脏伤口愈合过程经历了从促炎到抗炎再到修复反应的演变，而心脏成纤维细胞在整个转变过程中是一个核心参与者。成纤维细胞通过经历与促炎、抗炎和产生疤痕相关的连续极化表型，反映了左心室梗死中所见的变化。每种表型转变的发展都取决于成纤维细胞进入的心肌梗死后环境。在这篇小综述中，我们总结了我们目前对心肌梗死后心脏成纤维细胞激活的认识，并强调了仍存在差距的关键领域。
