Fibroblasts in myocardial infarction: a role in inflammation and repair.
Fibroblasts in myocardial infarction: a role in inflammation and repair.
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DOI：
10.1016/j.yjmcc.2013.11.015
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发表时间：
2014-05
影响因子：
5
通讯作者：
Frangogiannis, Nikolaos G.
中科院分区：
文献类型：
--
作者：
Shinde, Arti V.;Frangogiannis, Nikolaos G.
关键词：
成纤维细胞不仅作为产生基质的修复细胞，而且在炎症和免疫反应、血管生成和肿瘤形成中表现出广泛的功能。成年哺乳动物的心肌含有大量的成纤维细胞，这些成纤维细胞在间质和血管周围的细胞外基质中相互交织。本文综述了心肌梗死后心脏成纤维细胞表型和功能的动态变化。梗死心脏中心肌细胞的广泛坏死引发强烈的炎症反应。在梗塞愈合的早期阶段，成纤维细胞成为促炎细胞，激活炎性体并产生细胞因子、趋化因子和蛋白酶。促炎细胞因子（如白细胞介素-1）延迟肌成纤维细胞转化，直到伤口清除死细胞和基质碎片。炎症浸润的消退与成纤维细胞迁移、增殖、基质蛋白合成和肌成纤维细胞转化相关。生长因子和基质细胞蛋白在愈合的增殖期肌成纤维细胞活化中起重要作用。成熟的交联瘢痕的形成与成纤维细胞的清除相关，因为对抑制信号的理解不足抑制了纤维化反应。然而，在非梗死重塑心肌中，局部成纤维细胞可响应于容量和压力超负荷而保持活化，并可促进间质纤维化。考虑到它们的丰富性，它们在心脏炎症和修复中的关键作用，以及它们参与心肌功能障碍和心肌梗死，心脏成纤维细胞可能是心脏重塑的关键治疗靶点。
Fibroblasts do not only serve as matrix-producing reparative cells, but exhibit a wide range of functions in inflammatory and immune responses, angiogenesis and neoplasia. The adult mammalian myocardium contains abundant fibroblasts enmeshed within the interstitial and perivascular extracellular matrix. The current review manuscript discusses the dynamic phenotypic and functional alterations of cardiac fibroblasts following myocardial infarction. Extensive necrosis of cardiomyocytes in the infarcted heart triggers an intense inflammatory reaction. In the early stages of infarct healing, fibroblasts become pro-inflammatory cells, activating the inflammasome and producing cytokines, chemokines and proteases. Pro-inflammatory cytokines (such as Interleukin-1) delay myofibroblast transformation, until the wound is cleared from dead cells and matrix debris. Resolution of the inflammatory infiltrate is associated with fibroblast migration, proliferation, matrix protein synthesis and myofibroblast conversion. Growth factors and matricellular proteins play an important role in myofibroblast activation during the proliferative phase of healing. Formation of a mature cross-linked scar is associated with clearance of fibroblasts, as poorly-understood inhibitory signals restrain the fibrotic response. However, in the non-infarcted remodeling myocardium, local fibroblasts may remain activated in response to volume and pressure overload and may promote interstitial fibrosis. Considering their abundance, their crucial role in cardiac inflammation and repair, and their involvement in myocardial dysfunction and arrhythmogenesis, cardiac fibroblasts may be key therapeutic targets in cardiac remodeling.
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影响因子：
20.1
作者：
Dobaczewski M;Bujak M;Li N;Gonzalez-Quesada C;Mendoza LH;Wang XF;Frangogiannis NG
通讯作者：
Frangogiannis NG
DOI：
10.2353/ajpath.2010.090759
发表时间：
2010-05
期刊：
The American journal of pathology
影响因子：
--
作者：
Dobaczewski M;Xia Y;Bujak M;Gonzalez-Quesada C;Frangogiannis NG
通讯作者：
Frangogiannis NG
影响因子：
3.2
作者：
Bujak, Marcin;Frangogiannis, Nikolaos G.
通讯作者：
Frangogiannis, Nikolaos G.
影响因子：
10.8
作者：
Camelliti, P;Devlin, GP;Green, CR
通讯作者：
Green, CR
DOI：
10.1152/ajpheart.00514.2007
发表时间：
2007-09-01
影响因子：
4.8
作者：
Banerjee, Indroneal;Fuseler, John W.;Baudino, Troy A.
通讯作者：
Baudino, Troy A.