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The effector cells and cellular mediators of immune system involved in cardiac inflammation and fibrosis after myocardial infarction
Author(s) -
Liu Yihai,
Xu Jiamin,
Wu Mingyue,
Kang Lina,
Xu Biao
Publication year - 2020
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.29732
Subject(s) - inflammation , myocardial infarction , immune system , medicine , fibrosis , chemokine , cardiac fibrosis , cardiac function curve , immunology , ventricular remodeling , cardiology , heart failure
The cardiac repair after myocardial infarction (MI) involves two phases, namely, inflammatory response and proliferative response. The former is an inflammatory reaction, evoked by different kinds of pro‐inflammatory leukocytes and molecules stimulated by myocardial necrosis, while the latter is a repair process, predominated by a magnitude of anti‐inflammatory cells and cytokines, as well as fibroblasts. Cardiac remodeling post‐MI is dependent on the balance of individualized intensity of the post‐MI inflammation and subsequent cardiac fibrosis. During the past 30 years, enormous studies have focused on investigating immune cells and mediators involved in cardiac inflammation and fibrosis, which are two interacting processes of post‐MI cardiac repair. These results contribute to revealing the mechanism of adverse cardiac remodeling after MI and alleviating the impairment of cardiac function. In this study, we will broadly discuss the role of immune cell subpopulation and the involved cytokines and chemokines during cardiac repair post‐MI, particular in cardiac inflammation and fibrosis.