Unus pro omnibus, omnes pro uno: A novel, evidence-based, unifying theory for the pathogenesis of endometriosis

Antonio Simone Laganà, Salvatore Giovanni Vitale, Francesca Maria Salmeri, Onofrio Triolo, Helena Ban Frangež, Eda Vrtačnik-Bokal, Eda Vrtačnik Bokal, Lily Stojanovska, Vasso Apostolopoulos, Roberta Granese, Vincenza Sofo
Medical hypotheses · 2017 · vol. 103 , pp. 10–20 · doi:10.1016/j.mehy.2017.03.032 · PMID:28571791 · W2603229157
article OA: green CC0 ⤵ 167 in-corpus citations
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⚙ AI-generated summary by claude@2026-06+body, 2026-06-06 ⓘ

This paper proposes a unifying theory for endometriosis pathogenesis, suggesting that deregulation of Wnt signaling during organogenesis may cause aberrant stem cell placement, which is then activated by immune cells and inflammatory factors.

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⚙ AI-generated deep summary by claude@2026-06, 2026-06-06 ⓘ

This paper proposes a unifying, evidence-based theory for endometriosis pathogenesis that aims to address limitations of Sampson’s retrograde menstruation model, including why a physiological process affects most women while endometriosis affects a minority, why foci can occur at distant sites, and reports of endometriosis in male patients. The authors hypothesize that deregulation of developmental genes—particularly Wnt/β-catenin pathway and Hox genes with cofactor Pbx1—during organogenesis leads to aberrant placement and maintenance of stem cells with ectopic endometrial phenotypes in quiescent niches, with post-pubertal estrogen-driven immune and inflammatory signaling (e.g., macrophage activation and cytokines), adhesion molecules, extracellular matrix metalloproteinases, and survival pathways (e.g., Bcl-2) supporting differentiation, proliferation, and survival. A key caveat is that the paper presents a hypothesis and relies on reported evidence for components of the proposed mechanisms rather than providing new experimental validation. This paper is centrally about endometriosis — it formulates a novel unifying theory for how endometriosis might originate via embryologic gene signaling, immune activation, and ectopic endometrial cell survival.

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Condition tags

endometriosis

MeSH descriptors

Endometriosis Endometrium Animals beta Catenin beta Catenin Bone Marrow Cells Bone Marrow Cells Cell Adhesion Molecules Cell Adhesion Molecules Cell Differentiation Cytokines Cytokines Endometriosis Endometriosis Endometrium Endometrium Female Homeodomain Proteins Homeodomain Proteins Humans

Citation neighborhood

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.

References (100)

Cited by (50)

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