Fibroblast contributions to ischemic cardiac remodeling.
Fibroblast contributions to ischemic cardiac remodeling.
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DOI：
10.1016/j.cellsig.2020.109824
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发表时间：
2021-01
影响因子：
4.8
通讯作者：
Small EM
中科院分区：
文献类型：
--
作者：
Burke RM;Burgos Villar KN;Small EM
心脏可以通过组织结构和功能的改变来响应增加的病理生理需求。这一过程称为心脏重塑，在心肌梗死(MI)后尤为明显，心肌梗死时冠状动脉阻塞会导致广泛的心肌死亡。心肌梗死后，坏死的组织被细胞外基质(ECM)取代，剩余的存活心肌细胞(CM)经历肥大生长。ECM沉积和心肌肥厚被认为是增加结构完整性和防止心脏破裂的适应性反应。然而，持续的ECM沉积会导致纤维瘢痕的形成，从而阻碍心脏顺应性，并可能导致致命性心律失常。心脏成纤维细胞(CFs)被认为是胶原和纤维连接蛋白等ECM分子的主要来源，尤其是在被病理信号激活后。CFS参与心肌梗死后心脏修复和重塑的多个阶段，包括对CM死亡的初始反应、免疫细胞(IC)募集和纤维化瘢痕的形成。本综述的目的是描述成纤维细胞如何在心肌梗塞后的愈合和重塑中做出贡献，重点是成纤维细胞如何与正在愈合的梗死瘢痕中的其他类型的细胞进行沟通。
The heart can respond to increased pathophysiological demand through alterations in tissue structure and function . This process, called cardiac remodeling, is particularly evident following myocardial infarction (MI), where the blockage of a coronary artery leads to widespread death of cardiac muscle. Following MI, necrotic tissue is replaced with extracellular matrix (ECM), and the remaining viable cardiomyocytes (CMs) undergo hypertrophic growth. ECM deposition and cardiac hypertrophy are thought to represent an adaptive response to increase structural integrity and prevent cardiac rupture. However, sustained ECM deposition leads to the formation of a fibrotic scar that impedes cardiac compliance and can induce lethal arrhythmias. Resident cardiac fibroblasts (CFs) are considered the primary source of ECM molecules such as collagens and fibronectin, particularly after becoming activated by pathologic signals. CFs contribute to multiple phases of post-MI heart repair and remodeling, including the initial response to CM death, immune cell (IC) recruitment, and fibrotic scar formation. The goal of this review is to describe how resident fibroblasts contribute to the healing and remodeling that occurs after MI, with an emphasis on how fibroblasts communicate with other cell types in the healing infarct scar .
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影响因子：
8
作者：
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通讯作者：
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