The role of inflammation, oxidative stress, angiogenesis, and apoptosis in the pathophysiology of endometriosis: Basic science and new insights based on gene expression

Mansooreh Samimi, Mohammad Hossein Pourhanifeh, Mehdizadehkashi A, Abolfazl Mehdizadehkashi, Eftekhar T, Tahereh Eftekhar, Zatollah Asemi
Journal of cellular physiology · 2019 · vol. 234(11) , pp. 19384–19392 · doi:10.1002/jcp.28666 · PMID:31004368 · W2936185298
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This review examines the roles of inflammation, oxidative stress, angiogenesis, and apoptosis in endometriosis pathophysiology and discusses molecular signaling pathways relevant to therapeutic strategies.

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Abstract

Endometriosis is a frequent and chronic illness in young women which could be defined by the existence of endometrial stroma and glands outside of the normal site of the lining of the uterus. It has painful symptoms. The advanced stage of endometriosis may lead to gynecological malignancies, such as ovarian cancer, and other complications, including infertility. However, its exact physiopathology is not well known. Recent studies have shown the possible roles of inflammation along with oxidative stress. Additionally, angiogenesis and apoptosis dysregulation contribute to endometriosis pathophysiology. Therapeutic strategies and continuing attempts, to conquer endometriosis should be done regarding molecular signaling pathways. Thus, the present review summarizes current studies and focuses on molecular mechanisms.

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Condition tags

endometriosisinfertility

MeSH descriptors

Endometriosis Inflammation Neovascularization, Pathologic Oxidative Stress Apoptosis Apoptosis Apoptosis Endometriosis Endometriosis Endometriosis Endometriosis Endometrium Endometrium Endometrium Endometrium Female Female Gene Expression Regulation, Neoplastic Gene Expression Regulation, Neoplastic Gene Expression Regulation, Neoplastic

Citation neighborhood (2-hop)

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. Outer rings show 2-hop neighbours — papers reached through the immediate citers/citees. [ collapse to 1-hop ]

References (100)

Cited by (50)

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License: CC0 · commercial use OK