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Endometrial regeneration is the cyclic physiological process by which the functional layer of the uterine lining is restored following menstruation, parturition, or surgical injury (Gargett et al., 2016). This process is characterized by rapid tissue remodeling, involving the proliferation of epithelial and stromal cells, extensive angiogenesis, and the activation of resident endometrial stem/progenitor cells located in the basal layer (Critchley et al., 2020). The primary physiological driver of this regeneration is estrogen, which acts through its receptors to trigger mitogenic pathways and prepare the uterus for embryo implantation (Santamaria et al., 2018). Pathological failure of this process results in conditions such as Asherman's syndrome or a persistently thin endometrium, both of which are major contributors to uterine factor infertility (Dreisler & Kjer, 2019). While 'endometrial regeneration' itself is a biological process rather than a single molecular target, it is the focus of various therapeutic interventions including high-dose estrogen therapy, growth factor administration (e.g., G-CSF), and regenerative medicine techniques like stem cell transplantation (Zheng et al., 2020). Understanding the molecular pathways governing this regeneration, such as the Wnt/beta-catenin and TGF-beta signaling pathways, is crucial for developing targeted treatments for menstrual disorders and infertility (Tan et al., 2022).
Modulation of the endometrial microenvironment through hormonal stimulation of the Estrogen Receptor, recruitment of bone marrow-derived stem cells, and induction of angiogenic factors to promote tissue regrowth.
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