ArticleJournal of cardiothoracic surgery2026
MiR-32-3p improves ISO induced AC16 myocardial cell injury by targeting ATF4.
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
backgroundPathological myocardial hypertrophy is a key risk factor for heart failure and cardiovascular death. MicroRNAs (miRNAs), as a key post transcriptional regulator of gene expression, play an increasingly important role in myocardial hypertrophy and injury. This study aimed to investigate the expression, function, and mechanism of miR-32-3p through the miR-32-3p/ATF4 axis in ISO induced injury of human AC16 cardiomyocytes.
methodsA cell injury model was established by treating AC16 cells with 1 µM ISO. miR-32-3p mimic/inhibitor were transfected. Gene expression levels were detected using qRT-PCR; cell proliferation was evaluated via the CCK-8 assay; the levels of inflammatory cytokines (IL-6, TNF-α, IL-1β) were detected by ELISA; changes in oxidative stress levels (MDA, SOD, ROS) were analyzed using reagent kits; and the binding site between miR-32-3p and ATF4 was predicted through TargetScanHuman.; The miR-32-3p/ATF4 target relationship was validated using dual luciferase assays.
resultsISO induced downregulation of miR-32-3p expression (P < 0.0001), inhibition of AC16 cell proliferation (P < 0.0001), upregulation of myocardial hypertrophy markers ANP and β-MHC, as well as increased levels of inflammatory cytokines IL-6, TNF-α, IL-1β and oxidative stress (all P < 0.0001). When the miR-32-3p mimic was added, these changes were reversed. The dual luciferase assay confirmed that bioinformatics predicted miR-32-3p to directly target the 3'UTR of ATF4. The rescue experiment showed that overexpression of ATF4 eliminated the protective effect of miR-32-3p (P < 0.05).
conclusionsmiR-32-3p alleviates ISO induced AC16 cell damage by targeting ATF4, regulating inflammation and oxidative stress.
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