Figure 1.

Schematic representation depicts how free fatty acids (FFA) enhance the generation of ROS by promoting lipid peroxidation and mitochondrial damage, which ultimately results in reduced ATP production and the initiation of mitophagy. Elevated levels of circulating FFA can lead to an excess influx of FFAs into hepatocytes. The excess FFAs undergo β-oxidation, generating ROS and causing damage to various cellular components, including mitochondria. Mitochondrial damage, in turn, leads to a reduction in ATP production. Additionally, the accumulation of damaged mitochondria stabilizes the mitophagy regulatory protein PTEN-induced protein kinase 1 (PINK1) and recruits the protein PARKIN from the cytosol. The PINK1-PARKIN protein complex facilitates the removal of damaged mitochondria through mitophagy. Reproduced with permission to modify from Yuanqiang Ma et al. [102].