Authors
Jing Zhang, Peiyue Zhang, Haiyin Liu, Qi Li, Mengting Zhang, Li Liu, Zishu Yang, Canran Lv, Ruonan Li, Chengzhi Zhang, Wenqiang Li, Wei Wang, Jun Yang, Shiqun Li, Jing Li, Cuiyuan Huang, Jian Yang
Published in
FASEB journal : official publication of the Federation of American Societies for Experimental Biology. Volume 40. Issue 18. Pages e72277. Sep 30, 2026.
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-/- mice exhibited significantly reduced levels of myocardial oxidative stress and apoptosis induced by I/R, improved cardiac function, and a smaller area of myocardial infarction. In summary, LILRB4 recruits SHP-1, enhancing oxidative stress by inhibiting the PI3K-Nrf2 pathway and promoting apoptosis by suppressing the STAT3 pathway, thereby aggravating MIRI.
PMID:
42747797
Bibliographic data and abstract were imported from PubMed on 17 Sep 2026.
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