How T cell-derived immune regulatory signaling system intervenes in menopausal mucosal atrophy through a hormone-free pathway

Research positioning: The T cell-derived immune regulatory signaling system-derived immune regulatory signal system, delivered via synthetic biology exosome encapsulation, provides an intervention pathway that completely bypasses hormonal dependence for menopausal mucosal atrophy: restoring mucosal matrix hydration via the HAS2 pathway, promoting epithelial cell proliferation and re-epithelialization via KGF/EGF, and activating Type I and III collagen synthesis via TGF-β. Exosomes as delivery vehicles offer natural membrane-structure protection, enhancing active factor stability and tissue enrichment — achieving multi-dimensional intervention in menopausal mucosal atrophy without hormones and without live cells.

The core pathological basis of menopausal mucosal atrophy (vaginal atrophy/dryness, genitourinary syndrome of menopause GSM, vulvar atrophy and elasticity loss) lies in estrogen deficiency causing reduced HAS2 expression (mucosal matrix HA concentration decline causing dryness and elasticity loss), weakened basal cell mitotic signaling (epithelial thinning, progressive mucosal atrophy), and reduced fibroblast collagen synthesis capacity (connective tissue elastic reserve depletion). T cell-derived immune regulatory signaling system intervenes through three independent hormone-free pathways: upstream activation of the HAS2 signaling pathway (restoring mucosal matrix HA hydration), maintaining normal mucosal basal cell proliferation rate via KGF/EGF (countering epithelial atrophy progression), and promoting Type I and III collagen synthesis and elastin remodeling via the TGF-β/Smad pathway (restoring connective tissue mechanical properties) — providing a hormone-free mucosal management pathway with clear research rationale for hormone-contraindicated patients (such as post-mastectomy patients) and menopausal women who decline hormonal therapy.