ArticleJournal of thrombosis and thrombolysis2026
miR-4443 alleviates myocardial injury in acute myocardial infarction by targeting and regulating TIMP2.
Article in Journal of thrombosis and thrombolysis, 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
Acute myocardial infarction (AMI) continues to be a leading cause of global morbidity and mortality, where adverse left ventricular remodeling and subsequent heart failure serve as primary determinants of long-term prognosis. This study aimed to delineate the expression pattern, clinical significance, and molecular mechanisms of miR-4443 in AMI. The study included 100 patients diagnosed with AMI and 100 normal healthy controls. Serum miR-4443 levels were measured by qRT-PCR, and their correlations with patient prognosis were analyzed by Kaplan-Meier curve and Cox regression analysis. To mimic ischemia-reperfusion injury in vitro, human AC16 cardiomyocytes underwent hypoxia/reoxygenation (H/R) treatment. MTT for cell viability, flow cytometry for apoptosis, and ELISA for TNF-α, IL-1β, and IL-6 levels were performed to determine the regulatory role of miR-4443. A bioinformatics analysis predicted the targeting relationship between miR-4443 and TIMP2, and this was validated by the dual-luciferase reporter assay. For matrix remodeling evaluation, MMP2 and MMP9 mRNA expressions were detected by qRT-PCR. The expression of miR-4443 in serum samples from AMI patients was significantly downregulated. The low levels of miR-4443 indicate a poor prognosis for AMI. During H/R injury, miR-4443 expression was downregulated in AC16 cells, its overexpression significantly rescued H/R-induced cell viability decline, increased apoptosis, inflammatory factor release, and upregulation of MMP2/MMP9 expression. TIMP2 was a direct target gene for miR-4443. Functional rescue experiments showed that overexpression of TIMP2 could reverse the protective effect of miR-4443 mimics on H/R injury in cells. Our findings demonstrate that miR-4443 is downregulated in AMI and exerts protective effects against H/R injury in cardiomyocytes, at least in part, through targeting TIMP2, suggesting that the miR-4443/TIMP2 axis may be a potential critical regulatory target in AMI. Further in vivo validation is warranted to substantiate its therapeutic potential.
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