Inhibition of VEGFR1 TK Signaling in Peritoneal Macrophages Suppresses Endometriosis Development
article
OA: diamond
CC0
AI-generated summary
Inhibition of VEGFR1 tyrosine kinase signaling in peritoneal macrophages reduced endometriosis development and neovascularization by increasing M1 macrophage polarization.
One-sentence paraphrase of the abstract; not a substitute for reading it. No clinical advice. How this works
Abstract
Background/Aim: Endometriosis is characterized by the accumulation of immune cells in endometrial lesions and the peritoneal cavity. Macrophages contribute to the growth and neovascularization of endometriotic lesions. Vascular endothelial growth factor receptor-1 (VEGFR1) is involved in neovascularization, while peritoneal macrophages (PMs) play a critical role in endometriosis development and establishment. We examined the role of VEGFR1 signaling in PMs during endometriosis development using a murine model of ectopic endometrial transplantation. Materials and Methods: Endometrial fragments from female wild-type (WT) or VEGFR1 tyrosine kinase-deficient (TK−/−) donor mice were implanted into the peritoneal walls of recipient mice, either in a WT→WT or TK−/−→TK−/− combination. On day 14 after endometrial transplantation, the implant size, neovascular growth-promoting factors, macrophage accumulation in the implants and peritoneal cavity, and cytokine production were assessed. PMs from WT or TK−/− mice were transferred into the peritoneal cavity of WT→WT mice and their effects were assessed. Results: Compared to WT→WT mice, TK−/−→TK−/− mice exhibited smaller implant sizes and reduced neovascularization, including angiogenesis and lymphangiogenesis. This was correlated with an increase in pro-inflammatory (M1) and a decrease in alternative (M2) large peritoneal macrophages (LPMs) within the peritoneal cavity. Transfer of TK−/−-PMs into the peritoneal cavity of WT→WT mice reduced endometriosis development and macrophage accumulation. This led to increased expression of M1 macrophage genes and decreased expression of M2 phenotype genes, compared to WT-PMs transfer. PMs from TK−/− mice exhibited increased M1-related and decreased M2-related gene expression. Conclusion: Deletion of VEGFR1 TK signaling in PMs suppressed endometriosis progression and neovascularization by increasing M1 LPMs. Specific inactivation of VEGFR1 TK signaling may represent a potential therapeutic target for the management of endometriosis.
My notes (saved in your browser only)
Condition tags
MeSH descriptors
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 (33)
- Angiogenesis lymphangiogenesis and neurogenesis in endometriosis via openalex
- Cell subtypes and immune dysfunction in peritoneal fluid of endometriosis revealed by single-cell RNA-sequencing via openalex
- Characterization of leukocyte subpopulations in the peritoneal fluid of women with endometriosis via openalex
- Efficacy of niclosamide on the intra‐abdominal inflammatory environment in endometriosis via openalex
- Endometriosis, a disease of the macrophage via openalex
- Inhibition of receptor activity–modifying protein 1 suppresses the development of endometriosis and the formation of blood and lymphatic vessels via openalex
- Inhibition of TP signaling promotes endometriosis growth and neovascularization via openalex
- Lymphangiogenesis induced by vascular endothelial growth factor receptor 1 signaling contributes to the progression of endometriosis in mice via openalex
- M1 macrophages as promising agents for cell therapy of endometriosis via openalex
- Macrophages Are Alternatively Activated in Patients with Endometriosis and Required for Growth and Vascularization of Lesions in a Mouse Model of Disease via openalex
- Macrophages inhibit and enhance endometriosis depending on their origin via openalex
- Peritoneal immune microenvironment of endometriosis: Role and therapeutic perspectives via openalex
- Possible involvement of signal transducer and activator of transcription-3 in cell–cell interactions of peritoneal macrophages and endometrial stromal cells in human endometriosis via openalex
- Prevalence of newly diagnosed endometriosis in women attending the general practitioner via openalex
- Rediscovering peritoneal macrophages in a murine endometriosis model via openalex
- Retrograde menstruation in healthy women and in patients with endometriosis. via openalex
- The Role of Peritoneal Macrophages in Endometriosis via openalex
- Vascular endothelial growth factor A and C gene expression in endometriosis via openalex
- Vascular endothelial growth factor is produced by peritoneal fluid macrophages in endometriosis and is regulated by ovarian steroids. via openalex
- VEGF Receptor 1-Expressing Macrophages Recruited from Bone Marrow Enhances Angiogenesis in Endometrial Tissues via openalex
- W2084947524 via openalex
- W2068714945 via openalex
- W3160296380 via openalex
- W4317567638 via openalex
- W2058368422 via openalex
- W2044224359 via openalex
- W1846755436 via openalex
- W4402406679 via openalex
- W2339681982 via openalex
- W4407625237 via openalex
- W2515667551 via openalex
- W2156261200 via openalex
- W2153484787 via openalex
Source provenance
- europepmc
- last seen: 2026-06-04T01:30:01.192114+00:00
- openalex
- last seen: 2026-06-04T00:00:01.174412+00:00
- pmc
- last seen: 2026-05-13T20:22:03.195721+00:00
- pubmed
- last seen: 2026-05-20T00:31:01.111174+00:00
License: CC0
· commercial use OK