TGFBR2 coordinates the endometrial response to estrogen, regulating endometrial hyperplasia and fertility.

Summary

Using a progesterone receptor–Cre conditional knockout, the authors define TGFBR2 as a coordinator of estrogen responses in endometrium, linking its signaling to regulation of endometrial hyperplasia and fertility. The work delineates receptor-specific roles within TGFβ signaling in uterine biology.

Key Findings

• Conditional endometrial deletion of TGFBR2 (via progesterone receptor–Cre) reveals TGFBR2 as a key coordinator of estrogen responses.
• TGFBR2 signaling is implicated in regulating endometrial hyperplasia.
• Loss or modulation of TGFBR2 impacts fertility outcomes in the mouse model.

Clinical Implications

While preclinical, mapping TGFBR2’s role may inform biomarkers and therapeutic strategies for endometrial hyperplasia, infertility, and potentially endometrial cancer prevention.

Limitations

• Mouse model findings may not fully extrapolate to human endometrium.
• Abstracted details on molecular and phenotypic endpoints are limited in the available text.

Future Directions

Validate TGFBR2-dependent pathways in human endometrial tissue and assess therapeutic modulation in models of hyperplasia and subfertility.