Smoking and endometriosis: A narrative review
Endometriosis is a chronic gynecological disorder affecting 6–10% of women of reproductive age. While its etiology is multifactorial, growing evidence suggests that tobacco smoking may contribute to its development and progression through inflammatory, oxidative, and hormonal mechanisms. This narrat...
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| Main Authors: | , , , |
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| Format: | Article |
| Language: | English |
| Published: |
European Publishing
2025-06-01
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| Series: | Tobacco Induced Diseases |
| Subjects: | |
| Online Access: | https://www.tobaccoinduceddiseases.org/Smoking-and-endometriosis-A-narrative-review,203429,0,2.html |
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| Summary: | Endometriosis is a chronic gynecological disorder affecting 6–10% of women of
reproductive age. While its etiology is multifactorial, growing evidence suggests
that tobacco smoking may contribute to its development and progression through
inflammatory, oxidative, and hormonal mechanisms. This narrative review examines
the relationship between tobacco smoking and endometriosis, integrating molecular
insights to clarify potential biological pathways and highlight areas for future
research. A search was conducted in PubMed/MEDLINE and Web of Science,
including only original research articles published in English. Studies on both
human and animal models were considered, without restrictions on participant
age, to provide a comprehensive overview of tobacco-related mechanisms in
endometriosis. Tobacco smoke components, such as nicotine and polycyclic aromatic
hydrocarbons, can initiate and sustain an inflammatory response, leading to the
release of pro-inflammatory cytokines and recruitment of immune cells. Tobacco
smoking also induces oxidative stress, disrupting cellular functions and damaging
DNA. Moreover, it can cause hormonal dysregulation and interfere with hormonerelated
signaling pathways. Epigenetic modifications, including DNA methylation and
histone modifications, can also be induced by tobacco smoking. These changes affect
the expression of genes involved in inflammation, cell proliferation, and hormone
signaling, contributing to the pathogenesis of endometriosis. Future research
should prioritize longitudinal studies with objective biomarkers to strengthen causal
inference. Studies integrating omics approaches can further clarify tobacco-induced
molecular alterations in endometriosis. Public health policies should incorporate
targeted smoking prevention and cessation programs for women at risk. |
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| ISSN: | 1617-9625 |