Endometrial receptivity is a transient and highly coordinated biological state regulated by hormonal, molecular, vascular, metabolic, and immune pathways that collectively enable embryo implantation. This narrative review aims to synthesize contemporary evidence on the mechanisms governing endometrial receptivity and the heterogeneous etiologies of thin endometrium. A comprehensive literature search of PubMed, Scopus, and Web of Science published between 1998 and 2025 identified studies addressing morphological, molecular, metabolic, immunological, and microbiota-related determinants of receptivity. Current evidence demonstrates that receptivity is orchestrated through the interplay of the HOXA10–LIF–αvβ3 integrin axis, angiogenic signaling, extracellular matrix dynamics, mitochondrial bioenergetics, and AMPK–mTOR–mediated cellular energy regulation. Thin endometrium represents not a simple proliferative deficiency but a multifactorial phenotype shaped by vascular insufficiency, downregulation of key receptivity markers, metabolic stress, oxidative imbalance, fibrosis, immune disruption, and alterations in the uterine microbiota.Mechanism–directed therapeutic strategies including sildenafil, granulocyte colony-stimulating factor, platelet-rich plasma, mesenchymal stem cell–based regeneration, antioxidants, folate supplementation, and ERA-guided personalized embryo transfer target these underlying biological phenotypes rather than endometrial thickness alone. Shifting from thickness–based evaluation to a phenotype- and mechanism-oriented clinical framework is essential for improving implantation and pregnancy outcomes in assisted reproductive technologies.
FİLİZ et al. (Sun,) studied this question.