ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2026
LILRB4 Recruits SHP-1 to Enhance Oxidative Stress and Apoptosis, Aggravating Myocardial Ischemia-Reperfusion Injury.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Ischemia-reperfusion (I/R) leads to high levels of ROS, leading to cell death. The role of leukocyte immunoglobulin-like receptor B4 (LILRB4) in MIRI is unclear, despite its importance in oxidative stress and apoptosis regulation. In this study, we found that cardiac overexpression of LILRB4 increased the oxidative stress levels, promoted the expression of apoptotic cascade proteins, exacerbated I/R-induced cardiac dysfunction and myocardial injury in rats. LILRB4 also exacerbated H/R-induced cardiomyocyte injury, oxidative stress, and apoptosis. LILRB4 specifically binds to SH2-containing protein tyrosine phosphatase 1 (SHP-1), inhibiting the PI3K-Nrf2 signaling pathway and suppressing STAT3 phosphorylation and activation in cardiomyocytes. Compared to wild-type (WT) mice, LILRB4
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