In response to myocardial infarction (MI), the wound healing response of the left ventricle (LV) comprises overlapping inflammatory, proliferative, and maturation phases, and the cardiac fibroblast is a key cell type involved in each phase. It has recently been appreciated that, early post-MI, fibroblasts transform to a proinflammatory phenotype and secrete cytokines and chemokines as well as matrix metalloproteinases (MMPs). Later post-MI, fibroblasts are activated to anti-inflammatory and proreparative phenotypes and generate anti-inflammatory and proangiogenic factors and extracellular matrix (ECM) components that form the infarct scar. Additional studies are needed to systematically examine how fibroblast activation shifts over the timeframe of the MI response and how modulation at different activation stages could alter wound healing and LV remodeling in distinct ways. This review summarizes current fibroblast knowledge as the foundation for a discussion of existing knowledge gaps.

响应心肌梗塞（MI），左心室（LV）的伤口愈合反应包括重叠的炎症，增生和成熟阶段，而心脏成纤维细胞是每个阶段涉及的关键细胞类型。最近已经认识到，MI后早期，成纤维细胞转化为促炎表型并分泌细胞因子和趋化因子以及基质金属蛋白酶（MMP）。心肌梗死后，成纤维细胞被激活为抗炎和修复性表型，并产生抗炎和促血管生成因子以及形成梗塞疤痕的细胞外基质（ECM）成分。还需要进行其他研究来系统地检查成纤维细胞活化如何在MI反应的时间范围内变化，以及在不同活化阶段的调节如何以不同的方式改变伤口的愈合和左室重塑。这篇综述总结了当前的成纤维细胞知识，作为讨论现有知识差距的基础。