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

Zhou Fang; Xiang Li; Junying Liu; Haekyung Lee; Louis Salciccioli; Jason Lazar; Ming Zhang

doi:10.1016/j.bbrep.2023.101434

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

Biochem Biophys Rep. 2023 Jan 26:33:101434. doi: 10.1016/j.bbrep.2023.101434. eCollection 2023 Mar.

Authors

Zhou Fang¹, Xiang Li¹, Junying Liu¹, Haekyung Lee¹, Louis Salciccioli², Jason Lazar², Ming Zhang^{1

3}

Affiliations

¹ Department of Anesthesiology, USA.
² Department of Medicine, SUNY Downstate Health Science University, 450 Clarkson Avenue, Brooklyn, NY, 11203, USA.
³ Department of Cell Biology, USA.

Abstract

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.

Keywords: C4BP, C4 binding protein; Cardiac fibrosis. 1; Complement C3; DTBT, door-to-balloon time; FB, Factor B; FH, Factor F; FI, Factor I; IR, ischemia/reperfusion; IRI, ischemia/reperfusion injury; Ischemia/reperfusion injury (IRI); MBL, mannose binding lectin; Necrosis; TCC, terminal complement complex.