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已发表论文
LincRNA-p21 在乙醇诱导性肝损伤中的双重作用及其纳米颗粒递送解决方案
Authors Wang S, Nie ZC, Liu Y, Zhang ZY, Feng YM, Wang C, Jiang J
Received 2 December 2025
Accepted for publication 4 February 2026
Published 14 February 2026 Volume 2026:21 577455
DOI https://doi.org/10.2147/IJN.S577455
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 2
Editor who approved publication: Professor Eng San Thian
Shun Wang,1 Zhao-Chao Nie,1 Yang Liu,2 Zhi-Yue Zhang,2 Yi-Min Feng,1 Chengwei Wang,3 Jun Jiang3
1Department of Clinical Laboratory, The Second Qilu Hospital of Shandong University, Jinan, Shandong, 250033, People’s Republic of China; 2NMPA Key Laboratory for Technology Research and Evaluation of Drug Products, Key Laboratory of Chemical Biology (Ministry of Education), Department of Pharmaceutics, School of Pharmaceutical Sciences, Cheeloo College of Medicine, Shandong University, Jinan, Shandong, 250012, People’s Republic of China; 3Department of Neurosurgery, The Second Qilu Hospital of Shandong University, Jinan, Shandong, 250033, People’s Republic of China
Correspondence: Jun Jiang, Department of Neurosurgery, The Second Qilu Hospital of Shandong University, Jinan, Shandong, 250033, People’s Republic of China, Email jiangjun@sdu.edu.cn Chengwei Wang, Department of Neurosurgery, The Second Qilu Hospital of Shandong University, Jinan, Shandong, 250033, People’s Republic of China, Email wangchengwei@sdu.edu.cn
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 m6A demethylation and lincRNA-p21 upregulation. However, we revealed a dual-edged sword function for lincRNA-p21 in ethanol-induced liver injury in mice. LincRNA-p21 reduced acute ethanol-induced cell injury by enhancing autophagy but exacerbated chronic ethanol-induced liver cell injury by increasing ferroptosis. In vivo and in vitro analyses showed favorable therapeutic effects of ferr-1/lincRNA-p21@NPs on ALD.
Conclusion: These results show that lincRNA-p21 affects autophagy and ferroptosis, and the ferr-1/lincRNA-p21@NP nanosystem can provide protection against ALD.
Keywords: alcoholic liver disease, LincRNA-p21, autophagy, ferroptosis, drug delivery systems
1Department of Clinical Laboratory, The Second Qilu Hospital of Shandong University, Jinan, Shandong, 250033, People’s Republic of China; 2NMPA Key Laboratory for Technology Research and Evaluation of Drug Products, Key Laboratory of Chemical Biology (Ministry of Education), Department of Pharmaceutics, School of Pharmaceutical Sciences, Cheeloo College of Medicine, Shandong University, Jinan, Shandong, 250012, People’s Republic of China; 3Department of Neurosurgery, The Second Qilu Hospital of Shandong University, Jinan, Shandong, 250033, People’s Republic of China
Correspondence: Jun Jiang, Department of Neurosurgery, The Second Qilu Hospital of Shandong University, Jinan, Shandong, 250033, People’s Republic of China, Email jiangjun@sdu.edu.cn Chengwei Wang, Department of Neurosurgery, The Second Qilu Hospital of Shandong University, Jinan, Shandong, 250033, People’s Republic of China, Email wangchengwei@sdu.edu.cn
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 m6A demethylation and lincRNA-p21 upregulation. However, we revealed a dual-edged sword function for lincRNA-p21 in ethanol-induced liver injury in mice. LincRNA-p21 reduced acute ethanol-induced cell injury by enhancing autophagy but exacerbated chronic ethanol-induced liver cell injury by increasing ferroptosis. In vivo and in vitro analyses showed favorable therapeutic effects of ferr-1/lincRNA-p21@NPs on ALD.
Conclusion: These results show that lincRNA-p21 affects autophagy and ferroptosis, and the ferr-1/lincRNA-p21@NP nanosystem can provide protection against ALD.
Keywords: alcoholic liver disease, LincRNA-p21, autophagy, ferroptosis, drug delivery systems