Identification and validation of cuproptosis-related genes for diagnosis and therapy in nonalcoholic fatty liver disease

Li, Jinquan; Zhang, Yi; Ma, Xiaohan; Liu, Ruiqi; Xu, Cuicui; He, Qin; Dong, Ming

doi:10.1007/s11010-024-04957-7

Mol Cell Biochem

2024

DOI: 10.1007/s11010-024-04957-7

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Identification and validation of cuproptosis-related genes for diagnosis and therapy in nonalcoholic fatty liver disease

Jinquan Li,

Yi Zhang,

Xiaohan Ma

et al.

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Cited by 3 publications

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Cuproptosis and Cu: a new paradigm in cellular death and their role in non-cancerous diseases

Yang,

Feng,

Zhao

2024

Apoptosis

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Cuproptosis and Cu: a new paradigm in cellular death and their role in non-cancerous diseases

Yang,

Feng,

Zhao

2024

Apoptosis

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Elucidating cuproptosis in metabolic dysfunction-associated steatotic liver disease

Li,

Qi,

Song

et al. 2024

Biomedicine & Pharmacotherapy

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Copper and liver fibrosis in MASLD: the two-edged sword of copper deficiency and toxicity

Lonardo,

Weiskirchen

2024

Metab Target Organ Damage

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Copper is a trace metal whose absence or deficiency can cause structural and functional alterations that can be corrected by copper administration. Copper excess is associated with significant liver toxicity, such as that seen in Wilson’s disease, which often exhibits liver steatosis and can be managed by copper sequestrants. Copper, due to its ability to either accept or donate electrons, is a cofactor in many physiological redox reactions, playing an essential role in cell energy homeostasis, detoxification of reactive oxygen species, and hepatic immunometabolism. Given these facts, it is reasonable to speculate that copper might be involved in the pathogenesis of liver fibrosis in the setting of metabolic dysfunction-associated fatty liver disease (MASLD). To address this research question, a narrative review of published studies was conducted, spanning from the needs, sources, and toxicity of copper to Menkes and Wilson’s disease. Most epidemiological studies have demonstrated that MASLD is associated with copper deficiency. However, several studies show that MASLD is associated with copper excess and very few conclude that copper is not associated with MASLD. Therefore, the putative pathomechanisms associating both copper excess and deficiency with MASLD development and progression are reviewed. In conclusion, epidemiological and pathogenic data support the notion that well-balanced copper homeostasis is a prerequisite for liver health. Accordingly, both copper excess and deficiency may potentially predispose to liver fibrosis via the development of MASLD. Therefore, studies aimed at restoring normal bodily stores of copper should be tailored according to precision medicine approaches based on the specific features of copper metabolism in individual MASLD patients.

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Identification and validation of cuproptosis-related genes for diagnosis and therapy in nonalcoholic fatty liver disease

Cited by 3 publications

References 31 publications

Cuproptosis and Cu: a new paradigm in cellular death and their role in non-cancerous diseases

Cuproptosis and Cu: a new paradigm in cellular death and their role in non-cancerous diseases

Elucidating cuproptosis in metabolic dysfunction-associated steatotic liver disease

Copper and liver fibrosis in MASLD: the two-edged sword of copper deficiency and toxicity

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