ArticleArteriosclerosis, thrombosis, and vascular biology2026
RIPK3 Protects Against Endothelial Activation and Vascular Permeability in a Mouse Model of Ischemia-Reperfusion Injury.
Article in Arteriosclerosis, thrombosis, and vascular biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Crosstalk between autophagy-dependent ferroptosis and PANoptosis in myocardial and cerebral ischemia-reperfusion injury: mechanisms and therapeutic implications.Frontiers in pharmacology · 2026Review
- Comprehensive analysis of genes associated with necroptosis and pyroptosis in intestinal ischemia-reperfusion injury.PloS one · 2025Article
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6 authors.
Funding
Abstract
backgroundRIPK3 (receptor-interacting protein kinase 3) has context-specific roles that are frequently associated with cellular damage and death. We previously found that hypoxia can trigger elevated levels of RIPK3 in endothelial cells (ECs), which contributes to lethal vascular rupture during mouse embryonic development. However, it is unknown whether elevated RIPK3 likewise compromises endothelial barrier function in adult vasculature under hypoxic conditions such as ischemia-reperfusion (I/R) injury.
methodsTwelve-week-old male and female littermate control or inducible EC-specific
results
conclusionsEndothelial RIPK3 suppresses EC activation and inflammation associated with IL-6 and VCAM-1 elevation to protect the vascular barrier in the context of intestinal I/R injury. Thus, endothelial RIPK3 plays surprisingly beneficial roles that reduce I/R injury-induced vascular dysfunction.
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