Mitochondrial dysfunction and oxidative stress in OSAHS and associated comorbidities: Mechanism and potential targeted therapeutic strategies.

Obstructive sleep apnea-hypopnea syndrome (OSAHS) is associated with multisystem comorbidities, including cardiovascular disease, metabolic disorders, and neurological, pulmonary, and kidney diseases. Current studies have revealed that the pathophysiology of OSAHS and its associated comorbidities is complex. However, chronic intermittent hypoxia-induced mitochondrial dysfunction and oxidative stress are considered to play an important role. In recent years, mechanisms of interaction between mitochondrial dysfunction and oxidative stress have gained attention and have emerged as important potential therapeutic targets. Future delivery systems may improve the tissue or mitochondrial targeting of investigational agents, although their efficacy and safety in OSAHS remain to be established. This review highlights the mutual reinforcement and positive feedback loop between mitochondrial dysfunction and oxidative stress, and provides an overview of the current research on associated therapeutic drugs, their novel delivery systems, and development potential. Our review aims to provide new ideas and methods for the treatment of OSAHS-associated comorbidities.