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Causal effects of gut microbiome on endometriosis: a two-sample mendelian randomization study
BACKGROUND: Previous studies have shown observational associations between the gut microbiota and endometriosis; however, the causal nature of such associations remains unclear. This study aimed to analyze the genetic causal relationship between the two. METHODS: A gut microbiome genome-wide associa...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10687921/ https://www.ncbi.nlm.nih.gov/pubmed/38037013 http://dx.doi.org/10.1186/s12905-023-02742-0 |
Sumario: | BACKGROUND: Previous studies have shown observational associations between the gut microbiota and endometriosis; however, the causal nature of such associations remains unclear. This study aimed to analyze the genetic causal relationship between the two. METHODS: A gut microbiome genome-wide association study conducted by the MiBioGen consortium was used as exposure data, and summary statistics of endometriosis were obtained from the FinnGen consortium R8 release data. Inverse variance weighted, MR-Egger, weighted median, weighted model, and simple model analyses were applied to examine the causal relationship, and sensitivity analyses were conducted to validate the robustness of the results. RESULTS: The results showed that, out of 211 gut microbiome taxa, Clostridiales_vadin_BB60_group, Oxalobacteraceae, Desulfovibrio, Haemophilus, and Holdemania had protective effects on endometriosis, while Porphyromonadaceae and Anaerotruncus might contribute to the development of endometriosis. Heterogeneity and pleiotropy analyses confirmed the robustness of the results. CONCLUSION: The two-sample Mendelian randomization analysis conducted in this study identified specific intestinal flora with a causal relationship with endometriosis at the genetic level, offering new insights into the gut microbiota-mediated development mechanism of endometriosis. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12905-023-02742-0. |
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