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Causal Effects of Circulating Inflammatory Proteins on Postmenopausal Atrophic Vaginitis in European Populations: A
Xianyang Hu1,2, Shuai Ruan3, Tianyu Zhong1,4
1Clinical Laboratory, Huadong Hospital, Fudan University, Shanghai, People's Republic of China.
International Journal of Women'S Health
|August 4, 2026
Summary
This study investigated inflammatory proteins and postmenopausal atrophic vaginitis (PAV). Certain proteins influence PAV risk, with TGFA showing a protective role in vaginal health.
Area of Science:
- Genetics and Immunology
- Proteomics
- Women's Health
Background:
- Postmenopausal atrophic vaginitis (PAV) is common and undertreated, primarily due to estrogen deficiency.
- The causal role of circulating inflammatory proteins in PAV pathogenesis is not well understood.
Purpose of the Study:
- To investigate the causal relationship between circulating inflammatory proteins and the risk of postmenopausal atrophic vaginitis (PAV).
- To identify specific inflammatory proteins that may influence PAV development and progression.
Main Methods:
- Utilized Mendelian randomization (MR) with genetic instruments for 91 inflammatory proteins and PAV outcome data from the FinnGen Consortium.
- Employed inverse-variance weighted (IVW) and other MR methods, with sensitivity analyses to assess robustness.
- Validated findings using transcriptomic data from vaginal tissue.
Main Results:
- Six inflammatory proteins were associated with PAV risk: CCL19 and IL12B (increased risk), and CXCL5, TNFRSF9, IL10RA, and TGFA (decreased risk).
- TGFA showed a protective effect, supported by significantly lower expression in atrophic vaginal tissue.
- Sensitivity analyses indicated no significant pleiotropy or heterogeneity.
Conclusions:
- Provides genetic evidence for a causal influence of circulating inflammatory proteins on PAV risk.
- TGFA is a key candidate, potentially involved in vaginal epithelial maintenance.
- Highlights inflammation as a contributor to PAV and suggests potential therapeutic targets, warranting further validation.