ArticleInternational journal of nanomedicine2026
LincRNA-p21: A Double-Edged Sword in Ethanol-Induced Liver Damage and Its Nanoparticle Solution.
Article in International journal of nanomedicine, 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: Background: Alcohol-related liver disease (ALD) is the leading cause of liver disease-related deaths globally, necessitating new treatments. This study investigates the role of long intergenic noncoding RNA (lincRNA)-p21 in ALD and explores therapeutic strategies for liver injury. Methods: We identified lncRNAs linked to ethanol-induced liver injury using the Gene Expression Omnibus (GEO) database. Experiments were conducted to assess the function of lincRNA-p21 in ALD both in vivo and in vitro. Autophagy was analyzed through electron microscopy, autophagic flow, and protein expression. Bioinformatics explored underlying mechanisms, focusing on m6A modification of lincRNA-p21 by ALKBH5 using RNA Immunoprecipitation (RIP) and meRIP-PCR. Ferroptosis was induced with erastin, and its levels were measured by cell ROS and viability. A nanoplatform-based system was developed to co-deliver a plasmid encoding lincRNA-p21 and a ferroptosis inhibitor. We developed a nanoplatform-based co-delivery system to deliver a plasmid encoding lincRNA-p21 and the ferroptosis inhibitor ferrostatin-1 (ferr-1/lincRNA-p21@NP) to the liver. Results: LincRNA-p21 protected liver cells against ethanol-induced injury by promoting autophagy. ALKBH5 mediated the m Conclusion: These results show that lincRNA-p21 affects autophagy and ferroptosis, and the ferr-1/lincRNA-p21@NP nanosystem can provide protection against ALD.
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