Aberrant mitochondria in endometriosis: From pathogenic mechanisms to therapeutic opportunities

Summary Endometriosis affects about 10% of women of reproductive age and is a major cause of chronic pelvic pain and infertility, yet current therapies often fail to provide lasting relief. Mitochondrial dysfunction has emerged as a potential key contributor that drives disease progression through metabolic reprogramming, oxidative stress (OS), and mitochondrial DNA (mtDNA) abnormalities. These alterations disrupt energy metabolism, promote ectopic cell survival under hypoxia, and increase oxidative damage. This review highlights mitochondrial failure as both a proposed driver and therapeutic target, discussing biomarkers and emerging interventions including antioxidants, metabolic modulation, oxidative phosphorylation (OXPHOS) inhibition, and bioactive substances.