ArticleJournal of clinical and translational hepatology2026
Serum miR-381-3p: Diagnostic Role and Mechanisms in Liver Transplant Ischemia-reperfusion Injury.
Article in Journal of clinical and translational hepatology, 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
Background and Aims: Hepatic ischemia-reperfusion (HIR) injury impairs outcomes post-liver transplantation. Therefore, we aimed to investigate the role and mechanism of miR-381-3p in HIR. Methods: The study enrolled 150 healthy controls, 82 non-HIR-injured patients, and 68 patients with HIR injury following liver transplantation. Clinical data were analyzed. Multivariate analysis identified HIR risk factors; the predictive value of miR-381-3p was assessed via receiver operating characteristic analysis. An Results: Serum miR-381-3p was significantly elevated in HIR compared with the other groups. miR-381-3p was the strongest independent HIR risk factor, which was confirmed by receiver operating characteristic analysis. H/R upregulated miR-381-3p. Inhibiting miR-381-3p counteracted H/R-induced decreased viability and increased apoptosis, inflammation, and oxidative stress. miR-381-3p directly bound to and suppressed JAK2 via its 3' untranslated region (validated by luciferase and RIP). Transfection of si-JAK2 abolished the protective effects of miR-381-3p inhibition. Conclusions: miR-381-3p exacerbates post-transplant HIR by directly targeting JAK2, amplifying inflammation and oxidative stress. Thus, our findings nominate serum miR-381-3p as a promising non-invasive biomarker and suggest its potential as a therapeutic target for mitigating HIR injury.
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