ArticleAngiogenesis2026
Critical role of endothelial regulator of G protein signaling 5 in postnatal angiogenesis.
Article in Angiogenesis, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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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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Authors and funding
5 authors.
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Abstract
aimsRegulator of G protein signaling 5 (RGS5) modulates G-protein coupled receptor (GPCR) signaling and is markedly upregulated in angiogenesis. However, its function in endothelial cells and its role in mediating postnatal angiogenesis remain unclear. The purpose of this study is to define the role of endothelial RGS5 in regulating VEGF signaling and angiogenesis. METHODS AND
resultsIn a hindlimb ischemia model, we found impaired postnatal angiogenesis, reduced perfusion recovery, and increased rates of auto-amputation in mice with either global or endothelial-specific deletion of Rgs5. Rgs5 deficiency in ECs led to reduced VEGFR2 phosphorylation at Tyr
conclusionEndothelial RGS5 is a critical regulator of VEGF signaling and postnatal angiogenesis. By attenuating SHP-1-mediated dephosphorylation of VEGFR2, RGS5 preserves VEGF signaling and angiogenesis. Targeting the RGS5-SHP-1 axis may be a useful therapeutic strategy for improving angiogenesis in response to ischemia.
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