Upregulated expression of NINJ1, a membrane-rupturing protein, in cardiac tissue in myocardial ischemia/reperfusion (I/R) injury in mouse and rat models

Abstract

Cardiomyocyte death induces irreversible injury during myocardial ischemia/reperfusion (I/R). Multiple regulated cell death programs including ferroptosis, necroptosis, and pyroptosis have been implicated in the pathogenesis of myocardial I/R injury. NINJ1 (Ninjurin-1) mediates plasma membrane rupture and loss of plasma membrane integrity during different lytic cell death mechanisms. Here, we found that, myocardial ischemia/reperfusion significantly increases NINJ1 expression transcriptionally in the heart tissue of both mice and rats. NINJ1 might hypothetically be a more critical therapeutic target in myocardial I/R injury, since it represents a common membrane-rupturing protein during most cell death programs, compared to specific proteins functioning in particular cell death mechanisms. Further mechanistic studies are needed to better understand the involvement of NINJ1 and NINJ1 – mediated plasma membrane rupture in myocardial I/R injury.

Keywords

NINJ1; ischemia; reperfusion; plasma membrane rupture; myocardial injury; isochemia/reperfusion; inflammation; cardiac tissue