ArticleFrontiers in immunology2024
Proangiogenic properties of complement protein C1q can contribute to endometriosis.
Article in Frontiers in immunology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- The role ofFrontiers in immunology · 2026Article
- Endometriosis: An Immunologist's Perspective.International journal of molecular sciences · 2025Review
- Update on the pathogenesis of endometriosis-related infertility based on contemporary evidence.Frontiers in endocrinology · 2025Review
- Endometriosis as an immune-mediated disease: pathogenetic mechanisms and therapeutic strategies.Frontiers in immunology · 2025Review
- Epigenetic regulation of complement C1Q gene expression.Frontiers in immunology · 2024Article
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Authors and funding
17 authors.
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Abstract
Endometriosis (EM) is defined as the engraftment and proliferation of functional endometrial-like tissue outside the uterine cavity, leading to a chronic inflammatory condition. While the precise etiology of EM remains elusive, recent studies have highlighted the crucial involvement of a dysregulated immune system. The complement system is one of the predominantly altered immune pathways in EM. Owing to its involvement in the process of angiogenesis, here, we have examined the possible role of the first recognition molecule of the complement classical pathway, C1q. C1q plays seminal roles in several physiological and pathological processes independent of complement activation, including tumor growth, placentation, wound healing, and angiogenesis. Gene expression analysis using the publicly available data revealed that C1q is expressed at higher levels in EM lesions compared to their healthy counterparts. Immunohistochemical analysis confirmed the presence of C1q protein, being localized around the blood vessels in the EM lesions. CD68
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