ArticleCardiovascular research2025
Endothelial c-REL orchestrates atherosclerosis at regions of disturbed flow through crosstalk with TXNIP-p38 and non-canonical NF-κB pathways.
Article in Cardiovascular research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.
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Who cites it
7 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Mechanopriming by vascular stiffness and phenotypic reprogramming by disturbed flow: mechanobiology and clinical translation in atherosclerosis.Frontiers in cardiovascular medicine · 2026Pooled it
- The arterial-venous continuum: bridging atherosclerosis and chronic venous disease through endothelial dysfunction.Internal and emergency medicine · 2026Review
- Inflammation in atherosclerosis: Drivers, mechanisms and therapies.Acta pharmaceutica Sinica. B · 2026Review
- TWIST1 drives endothelial-to-mesenchymal-transition to stabilize atherosclerotic plaques.Nature communications · 2026Article
- Pathological mechanisms and research progress of multilevel intervention therapy for coronary heart disease.Frontiers in immunology · 2026Review
- Extracellular vesicles derived from menstrual blood-derived mesenchymal stem cells suppress inflammatory atherosclerosis by inhibiting NF-κB signaling.BMC medicine · 2025Article
- It is all c-RELative: a new perspective for a member of the nuclear factor kappa B family.Cardiovascular research · 2025Article
Corrections and comments
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Authors and funding
13 authors.
Funding
Abstract
aimsAtherosclerosis initiation at sites of disturbed blood flow involves heightened inflammation coupled to excessive endothelial cell (EC) proliferation. Here, we unveil the pivotal role of c-REL, a member of the NF-κB transcription factor family, in orchestrating these processes by driving dual pathological inflammatory and cell cycle pathways. METHODS AND
resultsAnalysis of cultured EC and murine models revealed enrichment and activation of c-REL at atherosusceptible sites experiencing disturbed flow. Transcriptome analysis, extensively validated in vitro and in vivo, demonstrates that endothelial c-REL drives inflammation via a TXNIP-p38 MAP kinase signalling pathway and enhances proliferation through a non-canonical NFKB2-p21 pathway. Consistent with its pivotal role in EC pathology, genetic deletion of c-Rel in EC significantly reduces plaque burden in hypercholesterolaemic mice.
conclusionThese findings underscore the fundamental role of c-REL in endothelial responses to disturbed flow and highlight therapeutic targeting of endothelial c-REL as a potential strategy for atherosclerosis treatment.
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Registered trials
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