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ABSTRACT Background Endometriosis is a challenging disease to treat and one of the leading causes of infertility. Impaired endometrial receptivity, and particularly inadequate decidualization of endometrial stromal cells (ESCs), is a crucial component. Multiple inflammatory factors disrupt decidualization. Methods A comprehensive search of PubMed and Google Scholar (peer‐reviewed journals only from 2000 to 2025) was performed in April 2025. The keyword “decidualization” was combined with “endometriosis”, “infertility”, and “inflammation”. We summarize recent findings regarding the mechanisms of endometrial receptivity, focusing on the decidualization of ESCs, and discuss the impact of endometriosis, particularly in relation to PG metabolism and the senescence‐associated secretory phenotype (SASP). Main Findings Endometriotic lesions demonstrate progesterone (P4) resistance and heightened inflammation due to elevated local estrogen levels and feedback loops involving PGE 2 and steroidogenic enzymes. Oxidative stress secondary to inflammation and menstrual blood in ectopic locations promotes lesion growth. Excessive numbers of senescent cells with SASP contribute to fibrosis in the lesions. Impaired decidualization also occurs in eutopic ESCs, which show epigenetic dysregulation and inflammation, and these have effects through P4 and PGE 2 signaling. Conclusion Both endometriotic lesions and eutopic endometrium in endometriosis patients exhibit changes that contribute to infertility, with abnormal inflammation and epigenetic modifications leading to impaired decidualization.
Tamura et al. (Wed,) studied this question.