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活性氧作为酒精性脂肪性肝病和非酒精性脂肪性肝病发病机制中的关键分子：未来展望

Reactive Oxygen Species as Key Molecules in the Pathogenesis of Alcoholic Fatty Liver Disease and Nonalcoholic Fatty Liver Disease: Future Perspectives.

作者信息

Zhang Zhiqing, Yang Hong, Han Fei, Guo Peng

机构信息

Department of Hepatobiliary Surgery, The Third Affiliated Hospital, Chongqing Medical University, Yubei, Chongqing 401120, China.

School of Public Health, Chongqing Medical University, Chongqing 400016, China.

出版信息

Curr Issues Mol Biol. 2025 Jun 17;47(6):464. doi: 10.3390/cimb47060464.

DOI:10.3390/cimb47060464
PMID:40699863
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12191510/
Abstract

Reactive oxygen species (ROS) are central to the progression of alcoholic fatty liver disease (ALD) and nonalcoholic fatty liver disease (NAFLD). In ALD, ROS arise from alcohol metabolism (CYP2E1 and ADH/ALDH2), causing oxidative damage and fibrosis. In NAFLD, mitochondrial dysfunction, ER stress, and lipotoxicity drive ROS overproduction due to metabolic dysregulation. Both diseases share ROS-mediated pathways, including mitochondrial/ER dysfunction, inflammation, and impaired lipid metabolism, accelerating steatosis to cirrhosis and cancer. Antioxidants, ER modulators, and lifestyle changes show therapeutic potential but require further clinical validation. Future research should leverage multi-omics and targeted therapies to optimize ROS-focused interventions for ALD and NAFLD.

摘要

活性氧（ROS）在酒精性脂肪性肝病（ALD）和非酒精性脂肪性肝病（NAFLD）的进展中起着核心作用。在ALD中，ROS源于酒精代谢（细胞色素P450 2E1和乙醇脱氢酶/乙醛脱氢酶2），导致氧化损伤和纤维化。在NAFLD中，由于代谢失调，线粒体功能障碍、内质网应激和脂毒性驱动ROS过度产生。这两种疾病都有ROS介导的途径，包括线粒体/内质网功能障碍、炎症和脂质代谢受损，加速脂肪变性发展为肝硬化和癌症。抗氧化剂、内质网调节剂和生活方式改变显示出治疗潜力，但需要进一步的临床验证。未来的研究应利用多组学和靶向治疗，以优化针对ALD和NAFLD的以ROS为重点的干预措施。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/961d/12191510/d82b5afdff9f/cimb-47-00464-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/961d/12191510/d6c770c6720a/cimb-47-00464-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/961d/12191510/6c8c05dfcec7/cimb-47-00464-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/961d/12191510/de6423b4666d/cimb-47-00464-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/961d/12191510/d82b5afdff9f/cimb-47-00464-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/961d/12191510/d6c770c6720a/cimb-47-00464-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/961d/12191510/6c8c05dfcec7/cimb-47-00464-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/961d/12191510/de6423b4666d/cimb-47-00464-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/961d/12191510/d82b5afdff9f/cimb-47-00464-g004.jpg

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[1]
Reactive Oxygen Species as Key Molecules in the Pathogenesis of Alcoholic Fatty Liver Disease and Nonalcoholic Fatty Liver Disease: Future Perspectives.

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本文引用的文献

[1]
Anti-inflammatory and antioxidant effects of anthocyanins in Nonalcoholic fatty liver disease (NAFLD): a systematic review of studies.

Crit Rev Food Sci Nutr. 2025-3-5

[2]
Cigarette smoking and alcohol-related liver disease.

Liver Res. 2024-12-5

[3]
MetALD: Clinical aspects, pathophysiology and treatment.

JHEP Rep. 2024-11-2

[4]
Cell-to-cell and organ-to-organ crosstalk in the pathogenesis of alcohol-associated liver disease.

eGastroenterology. 2024-10

[5]
Caveolin-1 ameliorates hepatic injury in non-alcoholic fatty liver disease by inhibiting ferroptosis via the NOX4/ROS/GPX4 pathway.

Biochem Pharmacol. 2024-12

[6]
Formononetin Induces Ferroptosis in Activated Hepatic Stellate Cells to Attenuate Liver Fibrosis by Targeting NADPH Oxidase 4.

Phytother Res. 2024-12

[7]
Thyroid hormone receptor-β analogues for the treatment of metabolic dysfunction-associated steatohepatitis (MASH).

J Hepatol. 2025-2

[8]
FITM2 deficiency results in ER lipid accumulation, ER stress, and reduced apolipoprotein B lipidation and VLDL triglyceride secretion in vitro and in mouse liver.

Mol Metab. 2024-12

[9]
Lipid nanoparticle encapsulated oleic acid induced lipotoxicity to hepatocytes via ROS overload and the DDIT3/BCL2/BAX/Caspases signaling in vitro and in vivo.

Free Radic Biol Med. 2024-9

[10]
Targeting chronic liver diseases: Molecular markers, drug delivery strategies and future perspectives.

Int J Pharm. 2024-7-20

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