Programmed cell death in adenomyosis: mechanisms and future perspectives

Islam Ahmed Abdelmawgood, Boushra MI, Michael Ibrahim Boushra
Molecular biology reports · 2026 · vol. 53(1) · doi:10.1007/s11033-026-12559-3 · PMID:42606793 · W7203646175
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This review summarizes recent advances in programmed cell death mechanisms, including apoptosis and ferroptosis, regarding their roles in the initiation and alleviation of adenomyosis to facilitate future therapeutic development.

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Abstract

Adenomyosis (ADM) is a common gynecological condition defined by the atypical invasion of endometrial-like structures, including glands and stroma, into the myometrium. ADM has been attributed to many etiologies, with substantial evidence supporting genetic, immunological, mechanical, and hormonal factors. Programmed cell death (PCD) is a distinct form of cell death, distinct from accidental cell death, and is characterized by specialized signaling pathways mediated by specific molecules. The normal process of cell death is essential for maintaining internal homeostasis and serves as a protective mechanism against biological or chemical harm. Numerous recent studies indicate that the progression of ADM is intricately associated with PCD pathways, including apoptosis, autophagy, pyroptosis, and ferroptosis. However, the functions of PCD in ADM have not been reviewed. This article summarizes recent advances and attributes of diverse forms of PCD in the initiation and alleviation of ADM. Investigating PCD in relation to ADM presents significant opportunities for future progress. A thorough understanding of the PCD mechanism in ADM could facilitate the development of innovative therapeutic approaches and delineate future research trajectories in the field.

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MeSH descriptors

Adenomyosis Adenomyosis Adenomyosis Adenomyosis Adenomyosis Adenomyosis Adenomyosis Adenomyosis Adenomyosis Adenomyosis Adenomyosis Adenomyosis Adenomyosis Adenomyosis Adenomyosis Adenomyosis Adenomyosis Adenomyosis Apoptosis Apoptosis

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Papers in the corpus that this work cites (lower rings, blue) and that cite this one (upper rings, green). Dot size scales with the paper's in-corpus citation count — bigger dot = more influential within the endo/adeno field. Click a dot to open that paper. [ expand to 2 hops ] — adds papers reached through this work's immediate citers/citees. Heavier; up to 60 extra dots.

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