IP3R2-mediated Ca²⁺ release promotes LPS-induced cardiomyocyte pyroptosis via the activation of NLRP3/Caspase-1/GSDMD pathway.

ABSTRACT: Pyroptosis plays a crucial role in sepsis, and the abnormal handling of myocyte calcium (Ca²⁺) has been associated with cardiomyocyte pyroptosis. Specifically, the inositol 1,4,5-trisphosphate receptor type 2 (IP3R2) is a Ca²⁺ release channel in the endoplasmic reticulum (ER). However, the specific role of IP3R2 in sepsis-induced cardiomyopathy (SIC) has not yet been determined. Thus, this study aimed to investigate the underlying mechanism by which IP3R2 channel-mediated Ca²⁺ signaling contributes to lipopolysaccharide (LPS)-induced cardiac pyroptosis. The SIC model was established in rats by intraperitoneal injection of LPS (10 mg/kg). Cardiac dysfunction was assessed using echocardiography, and the protein expression of relevant signaling pathways was an

SUBMITTER: Wu QR 

PROVIDER: S-EPMC10879485 | biostudies-literature | 2024 Feb

REPOSITORIES: biostudies-literature