Pathophysiology of Endometriosis: Insights from Immunohistochemical Analysis of Ectopic and Eutopic Tissues
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⤵ 4 in-corpus citations
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Immunohistochemical analysis reveals distinct differences in inflammatory markers, adhesion molecules, and cell cycle regulators between ectopic and eutopic endometrial tissues, providing insights into endometriosis pathophysiology.
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Abstract
Endometriosis is a complex gynecological disorder characterized by the presence of endometrial-like tissue outside the uterus, leading to chronic pain and infertility. Immunohistochemistry (IHC) serves as a vital technique for elucidating the molecular and cellular differences between ectopic endometriotic tissues and eutopic endometrium. IHC reveals significant variations in the expression of inflammatory markers, adhesion molecules, and cell cycle regulators. This literature review compiles findings from various studies that assess the role of key proteins, such as leukemia inhibitory factor (LIF), cyclooxygenase-2 (COX-2), and b-cell lymphoma 2 (BCL-2), across different menstrual phases and lesion types. Notably, elevated LIF levels and increased mast cell activity in ectopic tissues underscore the inflammatory landscape of endometriosis. Additionally, altered expression of adhesion molecules like integrins and cluster of differentiation 44 (CD44) suggests modified cellular interactions, while apoptotic markers reveal a survival advantage for ectopic cells. These insights enhance our understanding of endometriosis pathophysiology.
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Cited by (4)
- Nerve fibers in endometriosis: pain pathogenesis and new approaches to diagnosis 2026
- Hypoxia-induced regulations of cell adhesion molecules and their implications for pathogenesis, diagnosis, and treatment of endometriosis 2026
- Gene co-expression network reveals key hub genes associated with endometriosis using bulk RNA-seq 2025
- Molecular pathogenesis of ovarian endometrioma: mechanistic insights and therapeutic implications 2025
Source provenance
- europepmc
- last seen: 2026-06-04T01:30:01.192114+00:00
- openalex
- last seen: 2026-06-04T00:00:01.174412+00:00
- pmc
- last seen: 2026-05-13T20:22:03.195721+00:00
- pubmed
- last seen: 2026-05-27T00:31:12.738895+00:00
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