Protein lipoylation: mitochondria, cuproptosis, and beyond
Cheng-Han Lin1, Yeh Chin1, Ming Zhou2
1Institute of Biochemistry and Molecular Biology, China Medical University, Taichung, Taiwan; Cancer Biology and Precision Therapeutics Center, China Medical University, Taichung, Taiwan; Graduate Institute of Biomedical Sciences and Research Center for Cancer Biology, China Medical University, Taichung, Taiwan.
None:
Protein lipoylation, a crucial post-translational modification (PTM), plays a pivotal role in mitochondrial function and emerges as a key player in cell death through cuproptosis. This novel copper-driven cell death pathway is activated by excessive copper ions binding to lipoylated mitochondrial proteins, disrupting energy production and causing lethal protein aggregation and cell death. The intricate relationship among protein lipoylation, cellular energy metabolism, and cuproptosis offers a promising avenue for regulating essential cellular functions. This review focuses on the mechanisms of lipoylation and its significant impact on cell metabolism and cuproptosis, emphasizing the key genes involved and their implications for human diseases. It offers valuable insights into targeting dysregulated cellular metabolism for therapeutic purposes.
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