International Journal of Drug Delivery Technology
Volume 16, Issue 5s

Endometrial Progesterone Receptor Expression in Normal and Polycystic Ovary Syndrome Conditions: Molecular Patterns, Fertility Outcomes, and Research Gaps

Dr Amit Patil1, Dr Hemant Deshpande2

1PhD scholar, D. Y. Patil Medical College, Pune, Maharashtra, India
2Professor and Head of the Department, Obstetrics and Gynaecology, D. Y. Patil Medical College, Pune, Maharashtra, India

ABSTRACT

Polycystic ovary syndrome (PCOS) is a leading cause of infertility, traditionally attributed to anovulation; however, growing evidence indicates that endometrial dysfunction also plays a critical role in impaired reproductive outcomes. Progesterone receptor (PR) isoforms, PR-A and PR-B, are key mediators of progesterone-driven changes essential for endometrial receptivity. This systematic review synthesized human studies published between 2010 and 2025 examining endometrial PR expression in women with PCOS compared to normal ovulatory controls. A comprehensive search across PubMed and ScienceDirect identified 306 studies, from which 20 met the inclusion criteria. Findings revealed consistent patterns of altered PR-A and PR-B expression in PCOS, including abnormal isoform ratios, impaired signaling pathways, and reduced downstream gene activation. These disruptions correlated with defective decidualization, aberrant implantation window dynamics, and poorer fertility outcomes. The review highlights the need for integrated molecular and clinical studies to clarify endometrial progesterone resistance and its implications for reproductive prognosis in PCOS.

Keywords: Polycystic ovary syndrome, progesterone receptor isoforms, endometrial receptivity, progesterone resistance

How to cite this article: Patil A, Deshpande H, Endometrial Progesterone Receptor Expression in Normal and Polycystic Ovary Syndrome Conditions: Molecular Patterns, Fertility Outcomes, and Research Gaps. Int J Drug Deliv Technol. 2026;16(5s): 296-308; DOI: 10.25258/ijddt.16.5s.38

Source of support: Nil

Conflict of interest: None