Advances in the Pathophysiology of Thin Endometrium

Area of Science:

• Reproductive Medicine
• Gynecology
• Cell Biology

Background:

• Thin endometrium (≤7 mm) is a significant cause of infertility, recurrent pregnancy loss, and failed embryo implantation.
• Understanding the underlying pathophysiological mechanisms is crucial for developing effective treatments.

Purpose of the Study:

• To review the current understanding of thin endometrium pathophysiology.
• To highlight emerging therapeutic approaches for improving endometrial receptivity.

Main Methods:

• Review of published studies on endometrial function and dysfunction.
• Analysis of molecular and cellular mechanisms contributing to thin endometrium.
• Evaluation of conventional and regenerative therapeutic strategies.

Main Results:

• Impaired uterine perfusion and reduced vascular endothelial growth factor (VEGF) hinder angiogenesis.
• Hypoxia, HIF-1α, and RhoA/ROCK pathways disrupt endometrial integrity.
• Immune dysregulation (cytokines, NK cells) and epigenetic changes (DNA methylation, miRNA) affect implantation genes (HOXA10).
• Conventional therapies show variable efficacy, while regenerative approaches (stem cells, PRP) offer promising potential.

Conclusions:

• Thin endometrium results from complex interactions involving vascular, cellular, immune, and epigenetic factors.
• Regenerative therapies represent a promising avenue for enhancing endometrial receptivity and reproductive outcomes.
• Further research is needed to optimize novel regenerative therapies and confirm their safety and efficacy.