Mechanistic insights into inflammatory cytokines in adenomyosis‑induced infertility (Review)

Adenomyosis (AM), an estrogen‑dependent chronic inflammatory disease with a rising incidence, has emerged as a major cause of infertility and reduced clinical pregnancy rates in reproductive‑aged women, severely impairing reproductive health and quality of life. The core pathological mechanisms of AM are closely linked to aberrant local expression of inflammatory cytokines, including interleukin (IL)‑6, C‑X‑C motif chemokine ligand 8 (CXCL8), IL1B, tumor necrosis factor‑α, NF‑κB, cyclooxygenase‑2 and TGF‑β, which disrupt the immune barrier at the endometrial‑myometrial junction. This disruption further breaks the critical balance between proinflammatory and anti‑inflammatory cytokines, ultimately fostering an immune microenvironment hostile to embryo survival. Concurrently, inflammatory cytokine‑activated cellular processes, including proliferation, invasion, tissue injury and repair, epithelial‑mesenchymal transition and fibrosis, further induce pathological neovascularization and impair blood perfusion in the junctional zone. These pathological changes, in turn, compromise endometrial receptivity and inhibit decidualization, ultimately resulting in implantation failure. Based on these mechanisms, key inflammatory cytokines such as IL‑6, CXCL8, IL1B and IL‑10 hold potential as diagnostic biomarkers for AM‑related infertility and provide a theoretical basis for developing fertility‑preserving therapies targeting the inflammatory cascade (such as IL‑6 receptor monoclonal antibodies and TGF‑β inhibitors). These findings offer new approaches to achieve the dual goals of lesion control and fertility preservation in clinical practice.