<p>Obstructive Sleep Apnea (OSA) can cause multi-system damage with a high disease burden and limited therapeutic options, and there is an urgent need to find new alternative treatments. The structural and functional impairment of the upper airway dilator muscles is an important pathogenic mechanism in OSA, characterized by significant abnormalities in mitochondrial structure and function, a shift from slow-twitch to fast-twitch muscle fibers, increased muscle fatigue, and progressive peripheral nerve damage. Mitochondria are the primary source of energy for muscle cells and neurons. Therefore, mitochondrial dysfunction is a significant factor in disrupting the structure and function of the upper airway dilator muscles in OSA. Peroxisome proliferator-activated receptor gamma coactivator-1 alpha (PGC-1α) plays an essential role in maintaining normal mitochondrial function. This article focuses on the central role of PGC-1α and its mechanisms in regulating mitochondrial biogenesis, mitochondrial dynamics, energy metabolism, lipid metabolism, oxidative stress, inflammation, and motor neuron activity in the upper airway dilator muscles. It summarizes existing therapeutic measures targeting PGC-1α in OSA and suggests that PGC-1α may be a potential therapeutic target for the upper airway dilator muscles in OSA, proposing directions for future research.</p>