The role of complement C3 in the outcome of regional myocardial infarction

被引：8

作者：

Fang, Zhou ^{[1
]}

Li, Xiang ^{[1
]}

Liu, Junying ^{[1
]}

Lee, Haekyung ^{[1
]}

Salciccioli, Louis ^{[3
]}

Lazar, Jason ^{[3
]}

Zhang, Ming ^{[1
,2
,4
]}

机构：

[1] Dept Anesthesiol, Brooklyn, NY USA

[2] Dept Cell Biol, Brooklyn, NY USA

[3] SUNY Downstate Hlth Sci Univ, Dept Med, 450 Clarkson Ave, Brooklyn, NY 11203 USA

[4] SUNY Downstate Hlth Sci Univ, Dept Anesthesiol, MSC6, 450 Clarkson Ave, Brooklyn, NY 11203 USA

来源：

BIOCHEMISTRY AND BIOPHYSICS REPORTS | 2023年 / 33卷

关键词：

Ischemia; reperfusion injury (IRI); Complement C3; Necrosis; Cardiac fibrosis; 1; PERCUTANEOUS CORONARY INTERVENTION; ST-ELEVATION; EJECTION FRACTION; HEART-FAILURE; REPERFUSION; ACTIVATION; MECHANISMS; MANAGEMENT; ISCHEMIA; IMMUNE;

D O I：

10.1016/j.bbrep.2023.101434

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Coronary heart disease leading to myocardial ischemia is a major cause of heart failure. A hallmark of heart failure is myocardial fibrosis. Using a murine model of myocardial ischemia/reperfusion injury (IRI), we showed that, following IRI, in mice genetically deficient in the central factor of complement system, C3, myocardial necrosis was reduced compared with WT mice. Four weeks after the ischemic period, the C3-/- mice had significantly less cardiac fibrosis and better cardiac function than the WT controls. Overall, our results suggest that innate immune response through complement C3 plays an important role in necrotic cell death, which contributes to the cardiac fibrosis that underlies post-infarction heart failure.

引用

页数：6

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