Molecular Mechanisms Underlying Adolescent Endometriosis and Advancements in Medical Management

In: Endometriosis in Adolescents · 2020 · pp. 157–171 · doi:10.1007/978-3-030-52984-0_5 · W3104675970
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Endometriotic lesions exhibit altered estrogen signaling, pro-inflammatory pathways, impaired immunity, and resistance to apoptosis, leading to disease progression and symptoms.

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This chapter reviews the molecular and cellular mechanisms proposed to underlie adolescent endometriosis, contrasting ectopic endometriotic lesions with eutopic endometrium and summarizing evidence on estrogen-mediated signaling, pro-inflammatory pathway activation, impaired cellular immunity, altered apoptosis resistance, neovascularization, and the failure of immune surveillance that supports chronic lesion progression. It also highlights accumulating evidence for epigenetic mechanisms and discusses symptom manifestations such as cyclic and acyclic pelvic pain, dysmenorrhea, bloating, and dyspareunia. A key caveat is that the chapter is a narrative synthesis rather than a single original study, so it does not provide new experimental data or quantify uncertainty across findings. This paper is centrally about endometriosis — it focuses on molecular/cellular mechanisms and medical management concepts specific to adolescent endometriosis.

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Abstract

Molecular and cellular features of ectopic endometriotic lesions differ from eutopic endometrium. Estrogen-mediated cell signaling is altered, and pro-inflammatory pathways develop in the local microenvironment along with impaired cellular immunity. A multitude of growth factors, cytokines, and angiogenic factors play a critical role. Refluxed endometrial cells eventually adhering, invading, and proliferating along with neovascularization result in progression to a disease state characterized by evasion of the immune surveillance system by ectopic endometrial tissue. This failure of natural clearance by the immune system and resistance to apoptosis by ectopic endometrial cells results in chronic progression of disease. There is increasing evidence for epigenetic mechanisms involved in the pathogenesis of endometriosis. The inflammation, scarring, and adhesions are symptomatically expressed as cyclic and acyclic pelvic pain, dysmenorrhea, bloating, and dyspareunia significantly compromising quality of life. An understanding of the complex pro-inflammatory pathways, hormonal influences, and underlying cellular and molecular mechanisms involved in the progression of adolescent endometriosis could facilitate future medical treatment that would decrease disease symptomatology. Access this chapter Tax calculation will be finalised at checkout Purchases are for personal use only Similar content being viewed by others

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Springer, Cham. https://doi.org/10.1007/978-3-030-52984-0_5 Download citation DOI: https://doi.org/10.1007/978-3-030-52984-0_5 Published: Publisher Name: Springer, Cham Print ISBN: 978-3-030-52983-3 Online ISBN: 978-3-030-52984-0 eBook Packages: MedicineMedicine (R0)

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