MicroRNA-223-3p/NLRP3 axis attenuates LPS-induced sepsis-like myocardial dysfunction by suppressing cardiomyocyte pyroptosis.
B, Z., X, L., Q, X., T, W., Y, S., N, A., X, Z., K, Z., Y, W., & Z, C. (2026). MicroRNA-223-3p/NLRP3 axis attenuates LPS-induced sepsis-like myocardial dysfunction by suppressing cardiomyocyte pyroptosis.. Molecular biology reports. https://doi.org/10.1007/s11033-026-12556-6
B Z, X L, Q X, T W, Y S, N A, et al. MicroRNA-223-3p/NLRP3 axis attenuates LPS-induced sepsis-like myocardial dysfunction by suppressing cardiomyocyte pyroptosis.. Molecular biology reports. 2026; doi: 10.1007/s11033-026-12556-6
B Z, X L, Q X, et al. MicroRNA-223-3p/NLRP3 axis attenuates LPS-induced sepsis-like myocardial dysfunction by suppressing cardiomyocyte pyroptosis.[J]. Molecular biology reports. 2026. DOI: 10.1007/s11033-026-12556-6.
@article{b2026,
author = {Zhang B and Li X and Xu Q and Wang T and Sun Y and Aji N and Zhou X and Zhao K and Wu Y and Cheng Z},
title = {MicroRNA-223-3p/NLRP3 axis attenuates LPS-induced sepsis-like myocardial dysfunction by suppressing cardiomyocyte pyroptosis.},
journal = {Molecular biology reports},
year = {2026},
doi = {10.1007/s11033-026-12556-6},
note = {PMID: 42573828},
}
TY - JOUR AU - Zhang B AU - Li X AU - Xu Q AU - Wang T AU - Sun Y AU - Aji N AU - Zhou X AU - Zhao K AU - Wu Y AU - Cheng Z TI - MicroRNA-223-3p/NLRP3 axis attenuates LPS-induced sepsis-like myocardial dysfunction by suppressing cardiomyocyte pyroptosis. T2 - Molecular biology reports PY - 2026 DO - 10.1007/s11033-026-12556-6 AN - PMID:42573828 ER -
BACKGROUND: Sepsis-induced cardiomyopathy (SIC), a life-threatening complication of sepsis that is characterized by myocardial inflammation and cardiomyocyte death, remains a critical clinical challenge. MicroRNA (miRNA) is involved in the development of SIC. However, the roles and underlying mechanisms of miR-223-3p and pyroptosis in SIC remain unclear. METHODS AND RESULTS: In vitro and in vivo LPS-induced sepsis-like myocardial dysfunction (SLMD) models were established in order to partially represent SIC. Assessments via CCK-8 assay, flow cytometry, qRT-PCR, Western blotting, immunofluorescence, histological staining, and transmission electron microscopy revealed that miR-223-3p overexpression significantly increased cardiomyocyte viability, reduced the marker levels of pyroptosis, improved cardiac function, and alleviated myocardial injury. In contrast, miR-223 knockout (KO) decreased cardiomyocyte viability, increased the marker levels of pyroptosis, aggravated heart failure, and induced cardiac damage. Mechanistically, miR-223-3p suppressed LPS-induced NLRP3 inflammasome activation and inhibited the LPS-induced interaction between caspase-1 and gasdermin D. Notably, upon treatment with NLRP3 siRNA or a GSDMD-targeting pyroptosis inhibitor disulfiram, miR-223-3p failed to exert additional protective effects against SLMD. CONCLUSIONS: These findings demonstrate that miR-223-3p attenuates LPS-Induced SLMD by inhibiting the NLRP3 inflammasome and cardiomyocyte pyroptosis.