Decoding androgen excess in polycystic ovary syndrome: Roles of insulin resistance and other key intraovarian and systemic factors

Figure 4 Mechanism diagram of activin, transforming growth factor-β signaling regulation, and suppressor of mothers against decapentaplegic pathway activation. A: The modulation of activin signaling by inhibin and follistatin. Activin promotes follicle-stimulating hormone synthesis and ovarian function through suppressor of mothers against decapentaplegic signaling pathways. Inhibin acts as an antagonist by binding to activin receptors via its co-receptor betaglycan, preventing activin from signaling. Follistatin neutralizes activin by directly binding to it, blocking its interaction with receptors; B: Transforming growth factor-β (TGF-β) is produced in a latent (inactive) form, bound to latent TGF-β binding proteins anchored in the extracellular matrix. When needed, TGF-β is activated and released from the extracellular matrix to bind its receptors on the cell surface, initiating signaling pathways. This system ensures that TGF-β acts only when required. TGF-β: Transforming growth factor-β; SMAD: Suppressor of mothers against decapentaplegic.