Endometrial extracellular matrix and fibrosis pathways

The endometrial extracellular matrix (ECM) and fibrosis pathways represent the integrated biological processes governing the structural composition and remodeling of the uterine lining. Under physiological conditions, the endometrial ECM undergoes dynamic turnover during the menstrual cycle, a process tightly regulated by matrix metalloproteinases (MMPs) and tissue inhibitors of metalloproteinases (TIMPs) [PMID: 23535143]. Pathological disruption of these pathways, frequently triggered by surgical trauma or infection, leads to the excessive accumulation of fibrous connective tissue, a condition known as endometrial fibrosis or Asherman syndrome [PMID: 30103557]. This fibrotic transformation is primarily driven by the transforming growth factor-beta (TGF-beta) signaling cascade, which promotes myofibroblast differentiation and collagen deposition [PMID: 32824111]. The resulting scar tissue can obliterate the uterine cavity, leading to menstrual dysfunction and infertility by preventing successful embryo implantation. Therapeutic strategies targeting these pathways often focus on inhibiting pro-fibrotic cytokines like TGF-beta or modulating the balance of ECM-degrading enzymes to restore normal tissue architecture [PMID: 29935124]. Clinical approaches have also explored the use of vasodilators and antioxidants to improve endometrial receptivity and reduce fibrotic markers [PMID: 21324350].

Other names

Endometrial fibrosisUterine fibrosis pathwaysEndometrial extracellular matrix remodelingIntrauterine adhesion pathwaysAsherman syndrome pathways

Inhibition of the TGF-beta/Smad signaling pathway to reduce myofibroblast activation, modulation of the MMP/TIMP ratio to promote ECM degradation, and enhancement of uterine blood flow to support tissue regeneration [PMID: 21324350, PMID: 32824111].