Targeting inflammation in endometriosis: emerging therapeutic options

Endometriosis is a chronic, estrogen-dependent inflammatory disease affecting up to 10% of reproductive-aged women. Current therapies are predominantly hormone-based and offer symptomatic relief without correcting the immune dysregulation and inflammation that drive lesion persistence, pain, and infertility.

This review summarizes emerging strategies that directly target inflammatory pathways in endometriosis. Key mechanisms involved in lesion survival and symptom generation include cytokine signaling (TNF-α, IL-1, IL-6), oxidative stress, immune-checkpoint dysregulation, and activation of the JAK/STAT pathway. Therapeutic approaches discussed comprise biologic agents (infliximab, etanercept, adalimumab, anakinra, tocilizumab), small-molecule JAK inhibitors (tofacitinib), and antioxidant compounds such as N-acetylcysteine, resveratrol, and vitamins C and E.

Targeting inflammation represents a promising shift in endometriosis management, particularly for women who do not respond to hormonal therapies or aim to conceive. Preclinical studies consistently demonstrate reductions in lesion size, inflammatory cytokines, oxidative stress, and neuroangiogenic signaling. Early clinical evidence - especially for TNF-α and IL-1 blockade and for N-acetylcysteine - suggests improvements in pain and, in selected cases, reproductive outcomes. Although preliminary, these findings support the rationale for inflammation-directed therapies. Future research should prioritize randomized trials, long-term safety and fertility assessment, and biomarker-guided patient stratification to identify responders and optimize precision use of these agents.