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ISSN 1001-5256 (Print)
ISSN 2097-3497 (Online)
CN 22-1108/R
Volume 42 Issue 6
Jun.  2026
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Article Contents

Regulatory mechanism of telomere in metabolic associated fatty liver disease and related targeted therapies

DOI: 10.12449/JCH260626
Research funding:

National Natural Science Foundation of China (82160866);

Science and Technology Plan Project of Guizhou Province (Guizhou Science and Technology base-ZK (2023) General 433);

Key Laboratory Construction Project of Higher Education in Guizhou Province (Guizhou Education Technology (2023)017);

Guizhou Provincial Scientific and Technological Research Project on Traditional Chinese Medicine and Ethnic Medicine (QZYY-2025-182);

2024 “Youth Sailing Program” Project of Guizhou University of Traditional Chinese Medicine (Guizhongyaokehe-QNYFZK (2024) No.12)

More Information
  • Corresponding author: YANG Mei, 908417289@qq.com (ORCID: 0009-0003-3563-4767)
  • Received Date: 2025-11-02
  • Accepted Date: 2025-12-09
  • Published Date: 2026-06-25
  • Metabolic associated fatty liver disease (MAFLD) is the most prevalent chronic liver disease worldwide, and its progression is closely associated with the development of liver fibrosis, liver cirrhosis, and even hepatocellular carcinoma. However, there is still a lack of effective therapies for MAFLD in clinical practice. Telomere is the protective structure at the end of chromosomes, and telomere shortening and functional impairment have been identified as one of the key factors regulating the pathological progression of MAFLD. This article systematically reviews the core mechanism of action of telomere regulation in MAFLD, including its molecular functions in nucleotide metabolism, oxidative stress, and epigenetic regulation, as well as its pathological effect in hepatocytes and hepatic stellate cells. In addition, this article explores the clinical prospects of telomeres as biomarkers and therapeutic targets for MAFLD, in order to provide a theoretical reference for improving the precise diagnosis and treatment system of MAFLD.

     

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