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ISSN 2097-3497 (Online)
CN 22-1108/R
Volume 41 Issue 12
Dec.  2025
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Article Contents

Research advances in the prevention and treatment of metabolic associated fatty liver disease by alleviating copper overload-induced mitochondrial dysfunction

DOI: 10.12449/JCH251223
Research funding:

Yunnan Provincial Department of Science and Technology Traditional Chinese Medicine Basic Research Joint Special Progra (202301AZ070001-040);

Yunnan Province Graduate High-Quality Course Medical Molecular Biology 

More Information
  • Corresponding author: YAO Zheng, yaozhmail@126.com (ORCID: 0000-0001-7322-0651)
  • Received Date: 2025-05-16
  • Accepted Date: 2025-08-01
  • Published Date: 2025-12-25
  • Copper is one of the essential trace elements in the human body and participates in mitochondrial respiration, energy metabolism, and antioxidant processes in the form of coenzymes or copper-containing proteins. Intracellular copper accumulation mainly manifests as abnormal copper accumulation within mitochondria, leading to abnormalities in mitochondrial morphology and function. the pathological process of metabolic associated fatty liver disease (MAFLD) is closely associated with mitochondrial dysfunction. Studies have confirmed that copper overload can promote the development and progression of MAFLD; however, there is still a lack of systematic summarization of the mechanisms by which copper overload induces mitochondrial dysfunction and leads to MAFLD and related advances in drug research. In this context, this article reviews the research advances in the mechanisms by which copper overload induces mitochondrial dysfunction and leads to MAFLD, as well as related advances in drug research, in order to provide a theoretical reference for further investigation and treatment of MAFLD.

     

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