The pathogenesis of cardiac fibrosis.

The pathogenesis of cardiac fibrosis.
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DOI:
10.1007/s00018-013-1349-6
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发表时间:
2014-02
影响因子:
8
通讯作者:
Frangogiannis, Nikolaos G.
Frangogiannis, Nikolaos G.
中科院分区:
生物学1区
文献类型:
--
作者:
Kong, Ping;Christia, Panagiota;Frangogiannis, Nikolaos G.

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Cardiac fibrosis is characterized by net accumulation of extracellular matrix proteins in the cardiac interstitium and contributes to both systolic and diastolic dysfunction in many cardiac pathophysiologic conditions. This review manuscript discusses the cellular effectors and molecular pathways implicated in the pathogenesis of cardiac fibrosis. Although activated myofibroblasts are the main effector cells in the fibrotic heart, monocytes/macrophages, lymphocytes, mast cells, vascular cells and cardiomyocytes may also contribute to the fibrotic response by secreting key fibrogenic mediators. Inflammatory cytokines and chemokines, reactive oxygen species, mast cell-derived proteases, endothelin-1, the renin/angiotensin/aldosterone system, matricellular proteins and growth factors (such as TGF-β and PDGF) are some of the best-studied mediators implicated in cardiac fibrosis. Both experimental and clinical evidence suggests that cardiac fibrotic alterations may be reversible. Understanding the mechanisms responsible for initiation, progression and resolution of cardiac fibrosis is crucial to design anti-fibrotic treatment strategies for patients with heart disease.
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