On the other hand, mitochondrial dysfunction and ubiquitin proteasome system imbalance are important molecular mechanisms involved in the occurrence and development of skeletal muscle atrophy, studies have reported that H. pylori primarily uses its CagA protein to increase the level of mitophagy, block autophagic flux, cause mitochondrial dysfunction and ubiquitin-proteasome system imbalance by regulating the activation of the NLRP3 inflammasome (Coombs et al., 2011; Chen D. et al., 2024; Ji et al., 2025). The gene discussed is S100A8; the disease is muscle atrophy.