Mitochondrial transplantation and platelet rich plasma for the treatment of non-alcoholic fatty liver disease

Table 1 Mitochondrial dysfunction and oxidative stress in liver diseases

Liver disease	Main pathological alterations	Role of oxidative stress	Role of mitochondrial dysfunction	Ref.
NAFLD	Hepatic lipid accumulation, mild inflammation, metabolic dysregulation, lipid accumulation, altered autophagy and mitochondrial quality control	Increased ROS production promotes lipid peroxidation and mild inflammatory response, oxidative stress contributes to progression toward NASH	Early mitochondrial damage affects lipid metabolism and redox balance, drives lipid dysregulation, impairs energy homeostasis, and alters mitochondrial turnover	Zheng et al[38], Dabravolski et al[39], and Trinchese et al[40]
NASH	Steatosis, inflammation, hepatocyte injury and fibrosis	ROS and RNS overproduction activate NF-κB and upregulate TNF-α, IL-1β, IL-6, IL-8	mtDNA release activates TLR9-mediated inflammation; mitochondrial damage enhances lipotoxicity and fibrosis	Simões et al[11], Rodrigues et al[28], and Carter-Kent et al[41]
HCC	Cell proliferation, somatic mutations, altered mitochondrial dynamics (fusion/fission, mitophagy)	ROS promote DNA damage and tumor progression, oncogenic signaling, and resistance to apoptosis	Mitochondrial dysfunction enhances Warburg effect	Chen et al[42] and Su et al[43]

NAFLD: Non-alcoholic fatty liver disease; NASH: Non-alcoholic steatohepatitis; HCC: Hepatocellular carcinoma; ROS: Reactive oxygen species; RNS: Reactive nitrogen species; IL: Interleukin; TNF-α: Tumor necrosis factor α; NF-kB: Nuclear factor-kappa B.