Ferroptosis in fallopian tube fibrosis: molecular mechanisms, pathological crosstalk, and therapeutic opportunities

Fallopian tube fibrosis is an important cause of tubal dysfunction and female infertility, but its molecular mechanisms and effective anti-fibrotic treatments remain incompletely defined. Ferroptosis is a regulated cell-death process characterized primarily by iron-dependent phospholipid peroxidation. Changes in ferroptosis-related markers, including GPX4, SLC7A11, reactive oxygen species (ROS), malondialdehyde (MDA), and intracellular iron, may support a ferroptotic phenotype but are not sufficient on their own to establish ferroptosis. This review summarizes current evidence linking chronic inflammation, oxidative stress, iron and lipid metabolism, and ferroptosis to fibrotic remodeling, with particular attention to fallopian tube disease. We further examine potential roles of epithelial cells, macrophages, fibroblasts, and hormone-related iron regulation. However, direct fallopian-tube-specific evidence remains limited, and most proposed connections between ferroptosis and tubal fibrosis are hypothesis-generating rather than established causal mechanisms. Potential ferroptosis inhibitors, iron chelators, natural compounds, and nanomaterial-based delivery strategies are therefore discussed as preclinical or conceptual approaches requiring validation in appropriate tubal models. This review highlights current evidence gaps and proposes priorities for cell-type-specific mechanistic studies and translational evaluation.