Cuproptosis as a Potential Therapeutic Target for Steatotic Liver Disease

TL;DR

This paper explores how copper overload and a new type of cell death called cuproptosis might be linked to fatty liver disease and could offer new treatment options.

Contribution

The paper introduces cuproptosis as a novel potential therapeutic target for steatotic liver disease.

Findings

Copper overload can lead to cellular toxicity and is linked to liver disease.

Cuproptosis is a newly identified form of programmed cell death triggered by excess copper.

The paper suggests cuproptosis could be a promising target for treating steatotic liver disease.

Abstract

Steatotic liver disease (SLD) has become one of the most prevalent chronic liver diseases, representing a significant health burden worldwide. The complex pathogenesis of SLD results in a lack of specific therapeutic targets and effective drug treatment modalities. Copper (Cu) is a trace element that plays a critical role in various physiological processes, particularly hepatic metabolism. Meanwhile, Cu overload can induce cellular toxicity, which is generally explained by its capacity to induce oxidative damage. In 2022, a novel form of programmed cell death, designated as cuproptosis, was identified. In essence, excess Cu ions bind to the lipoylated components of the tricarboxylic acid cycle, resulting in proteotoxic stress and subsequent cell death. The role of cuproptosis in the pathologies of Cu overload-induced diseases has gained considerable attention. However, the association between SLD and Cu overload, particularly cuproptosis, remains to be elucidated. This review provides a concise overview of cuproptosis. The significance of Cu overload in SLD, as well as the potential association between cuproptosis and SLD, is explored. This review aims to offer insights into the potential of cuproptosis as a therapeutic target for SLD.

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