Endometrial Adult/Progenitor Stem Cells: Pathogenetic Theory and New Antiangiogenic Approach for Endometriosis Therapy

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Endometrial stem cells in the abdominal cavity may proliferate and differentiate into ectopic implants, contributing to endometriosis persistence and recurrence, suggesting antiangiogenic therapies and stem cell targeting as new treatment approaches.

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The paper develops an etiopathogenetic theory of endometriosis centered on the retrograde menstrual transport of endometrial cells, proposing that adult endometrial stem/progenitor cells (MSC-like) can proliferate, invade, and differentiate in ectopic sites to generate persistent implants. It argues that because only differentiated endometrial cells have steroid hormone receptors, stem/progenitor cells could underlie persistence and recurrence after therapies that induce hypoestrogenism, with MSC-driven angiogenesis further supporting survival and growth. A key limitation is that the work is largely theoretical and synthesis-based, relying on conceptual links rather than presenting new experimental data within the text provided. This paper is centrally about endometriosis — it proposes stem/progenitor cell mechanisms and an antiangiogenic therapeutic approach targeting endometriosis-related MSCs.

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Abstract

The cyclical arrival of endometrial cells into the abdominal cavity through retrograde flux at menstruation represents the etiopathogenetic basis of endometriosis. The endometrium has peculiar regenerative properties linked to the presence of adult stem cells similar to mesenchymal stem cells (MSCs). Once in the abdominal cavity, these MSCs could proliferate, invade, and differentiate into endometrial cells, finally generating ectopic implants. As only differentiated endometrial cells, and not endometrial MSCs, possess steroid hormone receptors, MSCs could be responsible for the high rate of persistence/recurrence of the disease after hypoestrogenism-inducing therapies. Even angiogenesis promoted by MSCs could play an important role, as survival and proliferation of endometriotic tissue depend on the formation of new blood vessels. Inhibition of angiogenesis represents, in fact, a new, promising therapeutic approach for the disease. Further, medications directly targeting endometriosis MSCs could be effective, alone or in association with hormonal treatments, in increasing the success of medical treatment.
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Abstract

The cyclical arrival of endometrial cells into the abdominal cavity through retrograde flux at menstruation represents the etio-pathogenetic basis of endometriosis. The endometrium has peculiar regenerative properties linked to the presence of adult stem cells similar to mesenchymal stem cells (MSCs). Once in the abdominal cavity, these MSCs could proliferate, invade, and differentiate into endometrial cells, finally generating ectopic implants. As only differentiated endometrial cells, and not endometrial MSCs, possess steroid hormone receptors, MSCs could be responsible for the high rate of persistence/recurrence of the disease after hypoestrogenism-inducing therapies. Even angiogenesis promoted by MSCs could play an important role, as survival and proliferation of endometriotic tissue depend on the formation of new blood vessels. Inhibition of angiogenesis represents, in fact, a new, promising therapeutic approach for the disease. Further, medications directly targeting endometriosis MSCs could be effective, alone or in association with hormonal treatments, in increasing the success of medical treatment. Similar content being viewed by others

References

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Sci. 21, 296–304 (2014). https://doi.org/10.1177/1933719113503405 Published: Issue date: DOI: https://doi.org/10.1177/1933719113503405

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endometriosis

MeSH descriptors

Adult Stem Cells Angiogenesis Inhibitors Endometriosis Endometrium Neovascularization, Pathologic Adult Adult Stem Cells Adult Stem Cells Angiogenesis Inhibitors Angiogenesis Inhibitors Animals Endometriosis Endometriosis Endometrium Endometrium Female Humans Neovascularization, Pathologic Neovascularization, Pathologic Niacinamide

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