Background and aim: Mitochondrial quality control (MQC) plays a significant role in the progression of liver fibrosis, with key processes such as mitochondrial fission, fusion, mitophagy and biogenesis maintaining mitochondrial homeostasis. To understand the molecular mechanisms underlying epigenetic regulation of mitochondrial quality control in liver fibrosis, with the aim of uncovering novel therapeutic targets for treating, mitigating, and potentially reversing liver fibrosis, in light of the most recent advances in this field.
Methods: We searched PubMed, Web of Science, and Scopus for published manuscripts using terms "mitochondrial quality control" "mitochondrial fission" "mitochondrial fusion" "mitochondrial biogenesis" "mitophagy" "liver fibrosis" "epigenetic regulation" "DNA methylation" "RNA methylation" "histone modification" and "non-coding RNA". Manuscripts were collated, studied and carried forward for discussion where appropriate.
Results: Mitochondrial fission, fusion, biogenesis, and mitophagy regulate the homeostasis of mitochondria, and the imbalance of mitochondrial homeostasis can induce liver fibrosis. Epigenetic regulation, including DNA methylation, RNA methylation, histone modifications, and non-coding RNAs, plays a significant role in regulating the processes of mitochondrial homeostasis.
Conclusion: Mitochondrial quality control and epigenetic mechanisms are intricately linked to the pathogenesis of liver fibrosis. Understanding these molecular interactions provides insight into potential therapeutic strategies. Further research is necessary to translate these findings into clinical applications, with a focus on developing epigenetic drugs to ameliorate liver fibrosis by modulating MQC and epigenetic pathways.
Keywords: Epigenetics; Liver fibrosis; Mitochondrial quality control; Molecular mechanisms.
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