Key result
miR-926-3p inhibition reduces myocardial injury in septic mice by enhancing autophagy via mTOR signaling.
Why the study?
The influence of miR-926-3p on myocardial injury and its underlying mechanisms in sepsis were not fully understood.
Does miR-926-3p inhibition ameliorate myocardial injury in septic mice?
Does miR-926-3p inhibition ameliorate myocardial injury in septic mice?
Inhibition of miR-926-3p ameliorates myocardial injury in septic mice by enhancing autophagy through regulation of the mTOR signaling pathway.
No clinical implications for sepsis yet; leaves open miR-926-3p inhibition as a myocardial target for translational research.
Background: The purpose of this study is to investigate the influence of miR-926-3p on myocardial injury and its mechanisms. Methods: An animal model of sepsis was constructed by CLP, and animals were randomly divided into 4 groups: C group, miR-926-3p inhibitor group, CLP + NC group, and CLP + miR-926-3p inhibitor group. Results: Compared with those in C group, echocardiographic parameters remarkably declined in CLP + NC group. Compared with CLP + NC group, miR-926-3p inhibitor group indicated elevated echocardiographic parameters in mice, pathological improvement tendency of myocardial tissues and distinct reduction in cardiomyocyte apoptosis. It could be observed by electron microscopy that the number of lysosomes in miR-926-3p inhibitor group was greatly increased relative to CLP + NC group. Immunofluorescence exhibited that the number of green fluorescent puncta was significantly higher in miR-926-3p inhibitor group as compared to that in CLP + NC group. The autophagic flow was verified by observing the relative expression of LC3II at different times. The results of Western blotting manifested that miR-926-3p inhibitor up-regulated mTOR-related protein expressions and down-regulated the protein expression of p-mTOR. LPS was adopted to induce cardiomyocyte injury in vitro, and the results confirmed that, identical to in vivo experiments, miR-926-3p inhibitor was able to up-regulate the protein expressions of mTOR-related protein and down-regulate p-mTOR protein expression in cardiomyocytes. After addition of MHY1485, The expression of mTOR-related proteins changes in each group. Conclusion: Inhibition of miR-926-3p enhances autophagy through regulation of the mTOR signaling pathway, thus ameliorating myocardial injury in septic mice.
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Yan et al. (2023) studied Sepsis-induced myocardial injury. miR-926-3p inhibitor vs. CLP + NC group was evaluated on Echocardiographic parameters, myocardial tissue pathology, and cardiomyocyte apoptosis. Inhibition of miR-926-3p ameliorated myocardial injury and reduced cardiomyocyte apoptosis in septic mice by enhancing autophagy through regulation of the mTOR signaling pathway.
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