ArticleProceedings of the National Academy of Sciences of the United States of America2014
Endothelial cell FGF signaling is required for injury response but not for vascular homeostasis.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 90 papers.
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Who cites it
90 citing papers in PubMed.
- Clinical proof of concept for anti-FGF2 therapy in exudative age-related macular degeneration (nAMD): phase 2 trials in treatment-naïve and anti-VEGF pretreated patients.Eye (London, England) · 2024Trial
- Review
- Recent advances in treating age-related macular degeneration and diabetic retinopathy: Current therapies and emerging novel approaches.GeroScience · 2026Review
- Skin capillary endothelial cells form a network of spatiotemporally conserved CaProceedings of the National Academy of Sciences of the United States of America · 2026Article
- Bemarituzumab Suppresses Choroidal Neovascularization in Mice by Downregulating Melanoma Cell Adhesion Molecule and Yes-Associated Protein 1.ACS pharmacology & translational science · 2026Article
- Skin capillary endothelial cells form a network of spatiotemporally conserved CabioRxiv : the preprint server for biology · 2026Article
- Environmental enrichment and physical exercise prevent stress-induced social avoidance and blood-brain barrier alterations via Fgf2.Nature communications · 2026Article
- A novel mutation in exon 18 ofThe Journal of international medical research · 2026Article
- Redox Regulation of Microvascular Physiology and Pathophysiology: Insights into Therapeutic Strategies and Limitations.Antioxidants & redox signaling · 2025Review
- WJOG18524G: a single-arm phase II study evaluating bemarituzumab combined with ramucirumab and paclitaxel in fibroblast growth factor receptor 2b (FGFR2b)-positive advanced gastric or gastroesophageal junction cancer (RAINBIRD).ESMO gastrointestinal oncology · 2025Article
- Angiopoietin-2 binds to FGFR2, inhibits FGF-FGFR2 signaling, and delays cutaneous wound healing by inhibiting wound angiogenesis.Angiogenesis · 2025Article
- Angiogenesis: Biological Mechanisms and In Vitro Models.Annals of biomedical engineering · 2025Review
- The Landscape of Vascular Endothelial Growth Factor Inhibition in Retinal Diseases.Investigative ophthalmology & visual science · 2025Review
- Sensory nerve-secreted factors regulate basal keratinocyte functionIntegrative organismal biology (Oxford, England) · 2025Article
- AIP1 Regulates Ocular Angiogenesis Via NLRP12-ASC-Caspase-8 Inflammasome-Mediated Endothelial Pyroptosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Tissue Engineered 3D Constructs for Volumetric Muscle Loss.Annals of biomedical engineering · 2024Review
- Review
- FGFR-targeted therapeutics: clinical activity, mechanisms of resistance and new directions.Nature reviews. Clinical oncology · 2024Review
- Safety and tolerability of intravitreal umedaptanib pegol (anti-FGF2) for neovascular age-related macular degeneration (nAMD): a phase 1, open-label study.Eye (London, England) · 2024Article
- Biology and therapeutic targeting of vascular endothelial growth factor A.Nature reviews. Molecular cell biology · 2023Review
30 more citing papers are in PubMed but not listed here.
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Authors and funding
16 authors.
Funding
Abstract
Endothelial cells (ECs) express fibroblast growth factor receptors (FGFRs) and are exquisitely sensitive to FGF signals. However, whether the EC or another vascular cell type requires FGF signaling during development, homeostasis, and response to injury is not known. Here, we show that Flk1-Cre or Tie2-Cre mediated deletion of FGFR1 and FGFR2 (Fgfr1/2(Flk1-Cre) or Fgfr1/2(Tie2-Cre) mice), which results in deletion in endothelial and hematopoietic cells, is compatible with normal embryonic development. As adults, Fgfr1/2(Flk1-Cre) mice maintain normal blood pressure and vascular reactivity and integrity under homeostatic conditions. However, neovascularization after skin or eye injury was significantly impaired in both Fgfr1/2(Flk1-Cre) and Fgfr1/2(Tie2-Cre) mice, independent of either hematopoietic cell loss of FGFR1/2 or vascular endothelial growth factor receptor 2 (Vegfr2) haploinsufficiency. Also, impaired neovascularization was associated with delayed cutaneous wound healing. These findings reveal a key requirement for cell-autonomous EC FGFR signaling in injury-induced angiogenesis, but not for vascular homeostasis, identifying the EC FGFR signaling pathway as a target for diseases associated with aberrant vascular proliferation, such as age-related macular degeneration, and for modulating wound healing without the potential toxicity associated with direct manipulation of systemic FGF or VEGF activity.
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