ArticleAngiogenesis2025
Mechanistic insights into endometriosis: roles of Streptococcus agalactiae and L-carnitine in lesion development and angiogenesis.
Article in Angiogenesis, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed.
- From local lesion to multisystem disease: integrated crosstalk among the gut microbiota, immune system, and host metabolism in endometriosis.Frontiers in immunology · 2026Review
- Gut microbiota-associated immunomodulation contributes to the protective effects of fluvastatin against endometriosis in a mouse model, accompanied by increasedFrontiers in microbiology · 2026Article
- From gut-reproductive microbiota to ferroptosis: a comprehensive insight into the molecular-pathogenicity of endometriosis.Frontiers in immunology · 2026Review
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Authors and funding
15 authors.
Funding
Abstract
Retrograde menstruation is a widely recognized etiological factor for endometriosis (EMs); however, it is not the sole cause, as not all affected women develop EMs. Emerging evidence suggests a significant association between the vaginal microbiota and EMs. Nonetheless, the precise mechanisms by which microbial communities influence the pathophysiology and progression of EMs remain unclear. In this study, the cervical mucus from patients with EMs showed significantly greater microbial abundance compared with that of controls, with Streptococcus agalactiae (S. agalactiae) exhibiting the most substantial increase as determined by 16S rRNA gene sequencing. In a murine model, elevated S. agalactiae levels significantly increased the lesion number and colonization, whereas antibiotic treatment reduced lesion formation. Metabolomic analyses showed elevated L-carnitine levels in the cervical secretions and serum of patients with EMs, a finding corroborated in murine tissues. Exogenous L-carnitine administration similarly increased the number and weight of endometriotic lesions. Meanwhile, the inhibition of L-carnitine synthesis suppressed lesion formation induced by S. agalactiae. In vitro, both S. agalactiae and L-carnitine promoted EMs cell proliferation, migration, and invasion. L-carnitine synthesis inhibition attenuated cell motility stimulated by S. agalactiae. Mechanistically, S. agalactiae enhanced angiogenesis through L-carnitine by upregulating vascular endothelial growth factor expression and increasing human umbilical vein endothelial cell motility. These findings identify S. agalactiae as a key cervical microbiome component in EMs development and reveal a microbiota-metabolite-angiogenesis axis that may offer novel therapeutic targets.
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Registered trials
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