Immune regulation of cardiac fibrosis post myocardial infarction.
Immune regulation of cardiac fibrosis post myocardial infarction.
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DOI:
10.1016/j.cellsig.2020.109837
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发表时间:
2021-01
影响因子:
4.8
通讯作者:
DeLeon-Pennell KY
中科院分区:
文献类型:
--
作者:
Zaidi Y;Aguilar EG;Troncoso M;Ilatovskaya DV;DeLeon-Pennell KY
Pathological changes resulting from myocardial infarction (MI) include extracellular matrix alterations of the left ventricle, which can lead to cardiac stiffness and impair systolic and diastolic function. The signals released from necrotic tissue initiate the immune cascade, triggering an extensive inflammatory response followed by reparative fibrosis of the infarct area. Immune cells such as neutrophils, monocytes, macrophages, mast cells, T-cells, and dendritic cells play distinct roles in orchestrating this complex pathological condition, and regulate the balance between pro-fibrotic and anti-fibrotic responses. This review discusses how molecular signals between fibroblasts and immune cells mutually regulate fibrosis post-MI, and outlines the emerging pharmacological targets and therapies for modulating inflammation and cardiac fibrosis associated with MI.
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通讯作者:
Lindsey, Merry L.
DOI:
10.1074/jbc.m111.324988
发表时间:
2012-04-20
期刊:
The Journal of biological chemistry
影响因子:
--
作者:
Chang MY;Chan CK;Braun KR;Green PS;O'Brien KD;Chait A;Day AJ;Wight TN
通讯作者:
Wight TN