ArticleJournal of cardiothoracic surgery2026
miR-222-3p targeting MEGF9 exacerbates sepsis-induced myocardial injury.
Article in Journal of cardiothoracic surgery, 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
backgroundSepsis-induced myocardial injury (SIMI) commonly occurs as a complication of severe sepsis and septic shock. This research aims to explore the function of miR-222-3p inhibition in SIMI and its possible regulatory mechanisms.
methodsA rat SIMI model was established using the cecal ligation and puncture method. In vitro experiments were conducted using lipopolysaccharide (LPS) to induce myocardial injury in H9C2 cells. miR-222-3p and MEGF9 expression were determined using qRT-PCR. Myocardial injury, inflammatory response, and oxidative stress indicators were detected using the ELISA and biochemical colorimetric assays. Cell viability and apoptosis were assessed using the CCK-8 method and flow cytometry. The interaction between miR-222-3p and MEGF9 was verified through a luciferase reporter gene assay.
resultsIn the serum of rats with sepsis and LPS-induced H9C2 cells, miR-222-3p exhibited high expression, while MEGF9 was lowly expressed. Inhibition of miR-222-3p alleviated myocardial injury, inflammatory response, and oxidative stress in sepsis rats and LPS-induced cells, as evidenced by reduced CK-MB, cTnI, LDH, IL-6, IL-1β, TNF-α, and MDA level, and enhanced SOD activity. Inhibition of miR-222-3p increased LPS-induced cell viability and diminished apoptosis. miR-222-3p targeted MEGF9. Inhibiting MEGF9 expression could reverse the protective role of miR-222-3p suppression on LPS-induced myocardial injury.
conclusionThis study's results indicate that miR-222-3p exacerbates SIMI reactions by targeting and inhibiting MEGF9 expression. It is possible that miR-222-3p functions as a potential therapeutic target for SIMI.
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