Table 1.

Mitochondrial functions in different chronic liver diseases.

	Steatotic Liver Disease (SLD) [26,27,28]	Metabolic Dysfunction-Associated SLD (MASLD/MAFLD) [29,30,31,32,33,34]	Excessive Alcohol and Metabolic-Associated SLD (MetALD) [35,36,37]	Drug-Induced Liver Injury (DILI) [38,39,40]
Mitochondrial structure	The electron transport chain (ETC) is disrupted; the activity of mitochondrial complex III is decreased.	Mitochondrial membrane permeability increases; cristae disappear and giant mitochondria appear; and membrane potential decreases.	Mitochondria swell; mitochondrial membranes rupture; and membrane potential disappears.	Mitochondrial outer membrane is damaged; mitochondrial membrane potential decreases.
Energy metabolism	ATP synthesis is inhibited; the TCA cycle is disrupted.	ATP synthesis is reduced; oxidative phosphorylation and fatty acid oxidation efficiency are reduced.	ATP synthesis is downregulated.	ATP deficiency; ETC is damaged; and succinic acid is accumulated.
Mitochondrial DNA (mt-DNA)	mt-DNA content and mitochondrial density increases.	The fragmentation of mt- DNA is increased; the frequency of mitochondrial mutations is increased.	The fragmentation of mt-DNA is increased.	The copy number of mitochondrial is reduced and mt-DNA is depleted.
Mitophagy	Mitophagy is reduced.	Mitophagy is reduced; mitochondrial quality control homeostasis is imbalanced; and mitochondrial fission is increased.	Excessive mitochondrial autophagy.	Mitochondrial selective autophagy is reduced.
mt-ROS	mt-ROS is increased, which is caused by incomplete oxidation of substrates such as succinic acid.	The increase in mt-ROS production is affected by diet, lifestyle, genes, etc.	mt-ROS increases via fat accumulation, etc.	mt-ROS increases.