ArticleHereditas2026
miR-1-3p, as a novel diagnostic and prognostic biomarker, aggravates pancreatic acinar cell injury in acute pancreatitis by targeting GNPTAB.
Article in Hereditas, 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
objectiveThe mechanisms underlying the progression of acute pancreatitis (AP) remain incompletely elucidated. This study investigates the expression pattern, diagnostic and prognostic value of miR-1-3p in AP patients, and further elucidates its role in pancreatic acinar cell injury and the underlying molecular mechanisms.
methodsmiR-1-3p levels were measured via qPCR and correlated with clinical indicators. ROC analysis evaluated diagnostic efficacy, and logistic regression assessed prognostic relevance. A Caerulein-induced injury model was established in MPC-83 cells. Post-transfection with a miR-1-3p inhibitor, cell viability (CCK-8), inflammatory factors (ELISA), and oxidative stress (WST-8/TBA) were evaluated. Bioinformatics-predicted target genes were validated through dual-luciferase reporter and RIP assays, with rescue experiments confirming the targeting relationship.
resultsmiR-1-3p was significantly upregulated in SAP patients and effectively distinguished healthy individuals (AUC = 0.880) and disease severity (AUC = 0.878). Its levels positively correlated with CRP, APACHE II, and BUN (p < 0.0001). High miR-1-3p expression independently predicted poor prognosis (OR = 9.54, p = 0.023). Inhibition of miR-1-3p alleviated Caerulein-induced cellular injury in vitro. GNPTAB was identified as a direct target, showing downregulation and negative correlation with miR-1-3p in patients. Rescue experiments confirmed that GNPTAB downregulation partially reversed the protective effects of miR-1-3p inhibition.
conclusionsmiR-1-3p, upregulated in SAP, is a potential diagnostic biomarker and predictor of poor prognosis. It exacerbates pancreatic acinar cell injury by targeting GNPTAB, contributing to inflammation, oxidative stress, and AP progression.
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