Endometriosis, subclinical cardiac remodeling, and cardiovascular risk: mechanistic insights from cardiac magnetic resonance and mediation analysis

Yanzhi Feng, Feng Y, Nie K, Kebing Nie, Mulun Xiao, Xiao M, Liu X, Xingyu Liu, Tong Wu, Zhang J, Jinjin Zhang, Wang S, Shixuan Wang
Reproductive biology and endocrinology : RB&E · 2026 · vol. 24(1) · doi:10.1186/s12958-026-01564-7 · PMID:42067936 · PMC13281489 · W7159824282
Observational OA: gold public-domain-us
📄 Open PDF Full text JSON View on OpenAlex View on PubMed View at publisher
⚙ AI-generated summary by gemini-2.5-flash-lite, 2026-06-10 ⓘ

Endometriosis is linked to increased cardiovascular disease risk and subclinical cardiac remodeling, primarily through metabolic and inflammatory pathways, as shown by UK Biobank data and cardiac magnetic resonance imaging.

One-sentence paraphrase of the abstract; not a substitute for reading it. No clinical advice. How this works

⚙ AI-generated deep summary by claude@2026-06, 2026-06-10 · read from full text ⓘ

Using UK Biobank data (6,158 women with endometriosis and 229,453 without) plus an external hospital cohort (612 laparoscopically confirmed cases with age-matched controls), the study assessed associations between endometriosis and cardiovascular disease outcomes via multivariable-adjusted Cox models, and evaluated cardiac magnetic resonance metrics for subclinical remodeling. Over a median 13-year follow-up, endometriosis was associated with higher risk of CVD (HR 1.18) and coronary heart disease (HR 1.25), with stroke also significantly increased in replication; CMR showed subclinical concentric remodeling such as greater interventricular septal thickness and relative wall mass. Mediation analyses incorporating 32 biomarkers indicated metabolic dysfunction as the dominant pathway, with triglyceride-glucose–related indices and lipid accumulation product contributing most, followed by inflammation and oxidative stress. The paper explicitly notes mechanism is inferred from mediation models rather than direct causal experiments, and it includes validation across cohorts but relies on observational data. This paper is centrally about endometriosis — it links endometriosis to increased cardiovascular risk and early subclinical cardiac remodeling using CMR and biomarker mediation analyses.

Read from the paper's body, not the abstract. Not a substitute for reading the paper. No clinical advice. How this works

Abstract

BACKGROUND: Endometriosis is a systemic gynecological disorder affecting ~ 10% of reproductive-aged women and shares pathophysiological features with cardiovascular disease (CVD). However, its associations with cardiac remodeling and CVD risk, as well as underlying mechanisms, remain unclear. METHODS: This study utilized data from the UK Biobank, comprising 6,158 women diagnosed with endometriosis and 229,453 women without the condition. To validate our results, we employed a hospital cohort from the Second Affiliated Hospital of the University of South China, which included 612 women with laparoscopically confirmed endometriosis and 612 age-matched controls. We applied multivariable-adjusted Cox proportional hazards models to investigate the association between endometriosis and the risk of CVD. Additionally, generalized linear models were used to evaluate cardiac magnetic resonance (CMR) metrics. Mediation analyses were conducted to quantify the contributions of 32 biomarkers, with a particular emphasis on metabolic indices (e.g., triglyceride-glucose (TyG)-related indices, lipid accumulation product (LAP)), inflammatory markers (C-reactive protein (CRP), inflammation score (INFLA)), oxidative stress indicators (urate, bilirubin), and hormonal status markers (sex hormone-binding globulin (SHBG)). RESULTS: Over a median 13-year follow-up, 23,239 CVD events occurred. Endometriosis was associated with increased risks of CVD (HR 1.18, 95% CI 1.09-1.29) and coronary heart disease (CHD) (HR 1.25, 95% CI 1.12-1.40). These findings were robust across multiple sensitivity analyses and consistently replicated in the external Chinese cohort, with an additional significant association observed for stroke (HR: 1.19, 95% CI: 1.03-1.40). CMR imaging revealed subclinical concentric remodeling, including increased interventricular septal thickness (1.11%, 95% CI 0.13-2.11), relative wall mass (1.11%, 95% CI 0.05-2.17), and septal-to-lateral wall thickness ratio (0.64%, 95% CI 0.00-1.29). Mediation analyses identified metabolic dysfunction as the primary pathway, with TyG-related indices (15.4%-17.3%), LAP (11.8%), and triglycerides (8.9%) accounting for the largest proportions, followed by inflammation (CRP: 11.1%; INFLA: 3.7%) and oxidative stress (urate: 6.0%). CONCLUSIONS: Endometriosis is associated with increased CVD risk and early subclinical cardiac remodeling, largely mediated by metabolic and inflammatory pathways. These findings underscore the necessity of cardiovascular risk stratification and metabolic monitoring in the clinical management of women with endometriosis.
Full text 5,893 characters · extracted from oa-html · 5 sections · click to expand

Abstract

Background Endometriosis is a systemic gynecological disorder affecting ~ 10% of reproductive-aged women and shares pathophysiological features with cardiovascular disease (CVD). However, its associations with cardiac remodeling and CVD risk, as well as underlying mechanisms, remain unclear.

Methods

This study utilized data from the UK Biobank, comprising 6,158 women diagnosed with endometriosis and 229,453 women without the condition. To validate our results, we employed a hospital cohort from the Second Affiliated Hospital of the University of South China, which included 612 women with laparoscopically confirmed endometriosis and 612 age-matched controls. We applied multivariable-adjusted Cox proportional hazards models to investigate the association between endometriosis and the risk of CVD. Additionally, generalized linear models were used to evaluate cardiac magnetic resonance (CMR) metrics. Mediation analyses were conducted to quantify the contributions of 32 biomarkers, with a particular emphasis on metabolic indices (e.g., triglyceride-glucose (TyG)-related indices, lipid accumulation product (LAP)), inflammatory markers (C-reactive protein (CRP), inflammation score (INFLA)), oxidative stress indicators (urate, bilirubin), and hormonal status markers (sex hormone-binding globulin (SHBG)).

Results

Over a median 13-year follow-up, 23,239 CVD events occurred. Endometriosis was associated with increased risks of CVD (HR 1.18, 95% CI 1.09–1.29) and coronary heart disease (CHD) (HR 1.25, 95% CI 1.12–1.40). These findings were robust across multiple sensitivity analyses and consistently replicated in the external Chinese cohort, with an additional significant association observed for stroke (HR: 1.19, 95% CI: 1.03–1.40). CMR imaging revealed subclinical concentric remodeling, including increased interventricular septal thickness (1.11%, 95% CI 0.13–2.11), relative wall mass (1.11%, 95% CI 0.05–2.17), and septal-to-lateral wall thickness ratio (0.64%, 95% CI 0.00–1.29). Mediation analyses identified metabolic dysfunction as the primary pathway, with TyG-related indices (15.4%–17.3%), LAP (11.8%), and triglycerides (8.9%) accounting for the largest proportions, followed by inflammation (CRP: 11.1%; INFLA: 3.7%) and oxidative stress (urate: 6.0%).

Conclusions

Endometriosis is associated with increased CVD risk and early subclinical cardiac remodeling, largely mediated by metabolic and inflammatory pathways. These findings underscore the necessity of cardiovascular risk stratification and metabolic monitoring in the clinical management of women with endometriosis. Highlights 1. Women with endometriosis face higher risks of cardiovascular disease, especially coronary heart disease. 2. CMR reveals subtle but significant adverse cardiac remodeling in women with endometriosis. 3. Metabolic dysfunction and systemic inflammation, notably TyG-related indices and LAP, predominantly mediate the link between endometriosis and cardiovascular risk. Similar content being viewed by others

Acknowledgements

We thank the UK Biobank (Application Number: 529233) and its participants, as well as the patients, clinicians, and staff at the Second Affiliated Hospital of University of South China for their important contributions to this study. Clinical trial number Not appliable. Funding This research was funded by the National Key Research and Development Program of China, grant number 2022YFC2704100 and the National Natural Science Foundation of China, grant number 82371648. Author information Authors and Affiliations Corresponding authors Ethics declarations Ethics approval and consent to participate This study was conducted in accordance with the Declaration of Helsinki. The UK Biobank received ethical approval from the North West Multi-centre Research Ethics Committee on 22 August 2006 (06/MRE08/65), with subsequent renewals every five years. For the external validation cohort, the study protocol was approved by the Institutional Review Board of the Second Affiliated Hospital of the University of South China (No. 2025006). Written informed consent was obtained from all participants prior to their inclusion in the study. Consent for publication Not appliable. Competing interests The authors declare no competing interests. Additional information Publisher’s Note Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations. Supplementary Information Rights and permissions Open Access This article is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License, which permits any non-commercial use, sharing, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if you modified the licensed material. You do not have permission under this licence to share adapted material derived from this article or parts of it. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by-nc-nd/4.0/. About this article Cite this article Feng, Y., Nie, K., Xiao, M. et al. Endometriosis, subclinical cardiac remodeling, and cardiovascular risk: mechanistic insights from cardiac magnetic resonance and mediation analysis. Reprod Biol Endocrinol (2026). https://doi.org/10.1186/s12958-026-01564-7 Received: Accepted: Published: DOI: https://doi.org/10.1186/s12958-026-01564-7

Text is read by the "Ask this paper" AI Q&A widget below. Extraction quality varies by source — PMC NXML preserves structure cleanly, OA-HTML may include some navigation residue, and OA-PDF can have broken hyphenation. The publisher copy (via DOI) is the canonical version.

My notes (saved in your browser only)

⚙ Ask this paper AI returns verbatim quotes from the full text · source: oa-html ⓘ

Answers must be backed by verbatim quotes from this paper's full text. Hallucinated quotes are dropped automatically; if no verbatim passage answers the question, we say so. How this works

Condition tags

endometriosis

MeSH descriptors

Cardiovascular Diseases Cardiovascular Diseases Cardiovascular Diseases Cardiovascular Diseases Cardiovascular Diseases Cardiovascular Diseases Cardiovascular Diseases Cardiovascular Diseases Cardiovascular Diseases Cardiovascular Diseases Cardiovascular Diseases Cardiovascular Diseases Cardiovascular Diseases Cardiovascular Diseases Cardiovascular Diseases Cardiovascular Diseases Cardiovascular Diseases Cardiovascular Diseases Cardiovascular Diseases Cardiovascular Diseases

Funding

funders
[{'doi': '10.13039/501100001809', 'name': 'National Natural Science Foundation of China', 'awards': ['82371648']}, {'doi': None, 'name': 'National Key Research and Development Program of China', 'awards': ['2022YFC2704100']}]

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 (1)

SciLite annotations

chemicals 6
triglyceride glucose lipid urate radical triglyceride urate radical

Source provenance

crossref
last seen: 2026-08-28T06:28:26.629433+00:00
europepmc
last seen: 2026-10-14T06:08:39.101224+00:00
openalex
last seen: 2026-08-01T06:00:24.223380+00:00
pubmed
last seen: 2026-10-14T06:03:52.985691+00:00
scilite
last seen: 2026-06-21T06:47:03.627287+00:00
unpaywall
last seen: 2026-05-11T08:34:28.763810+00:00
License: public-domain-us · commercial use OK · attribution required
Courtesy of the U.S. National Library of Medicine