The role of growth factors in the pathogenesis of endometriosis
This review examines the abnormal expression of growth factors in endometriosis patients and their role in disease pathogenesis and hormonal regulation.
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This literature review examines how growth factors and their abnormal expression, regulation by hormonal status, and downstream signaling may contribute to endometriosis pathogenesis, drawing together evidence on factors, receptors, and immune–inflammatory pathways. It highlights specific examples including elevated TGF-β in peritoneal fluid and other compartments, potential TGF-β1–mediated impairment of NK-cell activity and resistance to apoptosis, and links to VEGF-driven angiogenesis with discussion of controversial VEGF concentration changes across the menstrual cycle. The paper also covers growth-factor control of cell-cycle progression (e.g., IGF-1/epidermal growth factor) and summarizes how VEGF isoforms differ in extracellular matrix binding and angiogenic potential. As a review, it is limited by reliance on heterogeneous prior studies and includes noted discrepancies, such as mouse data where TGF-β1 deletion did not alter proliferation or vessel density in lesions. This paper is centrally about endometriosis — it reviews the roles of growth factors (notably TGF-β, VEGF, and IGF pathways) in endometriosis development.
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