In Search of Pathogenic Mechanisms in Endometriosis: The Challenge for Molecular Cell Biology

A Starzinski-Powitz, Anna Starzinski‐Powitz, Starzinski-Powitz A, Andreas Zeitvogel, A Zeitvogel, Zeitvogel A, Schreiner A, A. Schreiner, R Baumann, R Baümann, Baumann R
Current Molecular Medicine · 2001 · vol. 1(6) , pp. 655–664 · doi:10.2174/1566524013363168 · PMID:11899254 · W2136358126
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⚙ AI-generated summary by gemini-2.5-flash-lite, 2026-06-09 ⓘ

This review discusses the cellular basis of endometriosis lesion formation, focusing on the potential role of a plastic founder cell population with self-renewal capacity that responds to host environment stimuli.

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This review paper discusses gaps in understanding the aetiology and pathogenesis of endometriosis, focusing on molecular and cellular mechanisms underlying lesion formation, and how cytokines and other factors may modulate these processes. It highlights that endometriosis shows tumour-like invasion and metastasis behaviors despite being non-neoplastic, and notes that causative therapy and non-invasive diagnostics are not available. The authors emphasize evidence and competing theories such as implantation via retrograde menstruation and a complementary “metaplasia” concept, and propose an endometriotic “founder” cell population with plasticity for differentiation and self-renewal as a potential explanation for how ectopic lesions establish in response to the host environment, while acknowledging the challenge posed by the debated, limited experimental information. This paper is centrally about endometriosis — it reviews cellular and molecular hypotheses for lesion initiation, founder-cell plasticity, and invasion/metastasis in endometriosis.

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Abstract

Endometriosis, defined histologically as the presence of endometrium-like glands and stroma outside the uterus, is a chronic, invasive and metastasising disease. It shares features with malignant tumours (invasion and metastasis) but is not neoplastic. Despite the fact that endometriosis is one of the most frequent gynaecological diseases, it is under researched, puzzling and highly debated. The aetiology and pathogenesis is little understood although it is agreed that implantation, at least in many cases, is responsible for endometriosis. This theory advocates retrograde menstruation as the underlying phenomenon, where cells of the menstrual efflux provide the cellular source for endometriotic lesion formation. Causative therapy and non-invasive diagnostics of endometriosis do not exist. Thus, there is a substantial but unmet need for molecular and cellular research to unravel the pathogenic mechanisms of endometriosis as a basis for developing novel diagnostic and therapeutic concepts. In this review, we specifically focus on the cellular basis of lesion formation, the possible modulation of this by cytokines and other factors and the characteristics of endometriotic cells in terms of invasion and metastasis. Considering available experimental information, we concentrate on arguments and ideas in favour of an endometriotic founder cell population exhibiting substantial plasticity for differentiation and self-renewal. Perhaps present in the menstrual efflux or arising by metaplasia (a complementary theory to implantation), this cell type might respond to stimuli present in the ectopic host environment and establish the endometriotic phenotype.
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Abstract

Endometriosis, defined histologically as the presence of endometrium-like glands and stroma outside the uterus, is a chronic, invasive and metastasising disease. It shares features with malignant tumours (invasion and metastasis) but is not neoplastic. Despite the fact that endometriosis is one of the most frequent gynaecological diseases, it is under researched, puzzling and highly debated. The aetiology and pathogenesis is little understood although it is agreed that implantation, at least in many cases, is responsible for endometriosis. This theory advocates retrograde menstruation as the underlying phenomenon, where cells of the menstrual efflux provide the cellular source for endometriotic lesion formation. Causative therapy and non-invasive diagnostics of endometriosis do not exist. Thus, there is a substantial but unmet need for molecular and cellular research to unravel the pathogenic mechanisms of endometriosis as a basis for developing novel diagnostic and therapeutic concepts. In this revi ew, we specifically focus on the cellular basis of lesion formation, the possible modulation of this by cytokines and other factors and the characteristics of endometriotic cells in terms of invasion and metastasis. Considering available experimental information, we concentrate on arguments and ideas in favour of an endometriotic founder cell population exhibiting substantial plasticity for differentiation and self-renewal. Perhaps present in the menstrual efflux or arising by metaplasia (a complementary theory to implantation), this cell type might respond to stimuli present in the ectopic host environment and establish the endometriotic phenotype.

Keywords

Pathogenic Mechanisms, E-cadherin, Plasticity of Mesenchymal, anti-apoptotic signals 9

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Condition tags

endometriosis

MeSH descriptors

Endometriosis Cell Differentiation Cytokines Cytokines Endometriosis Endometriosis Endometriosis Endometriosis Epithelial Cells Epithelial Cells Female Humans Mesoderm Mesoderm Metaplasia Models, Biological Molecular Biology Phenotype

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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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