ArticleCirculation research2015
Receptor-interacting protein kinase 3 contributes to abdominal aortic aneurysms via smooth muscle cell necrosis and inflammation.
Article in Circulation research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 82 papers.
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Who cites it
82 citing papers in PubMed, 130 citations in OpenAlex.
- Predicting Abdominal Aortic Aneurysm Progression: The Role of 18F-Fluorodeoxyglucose Aortic Wall Uptake and Flow Dynamics.Life (Basel, Switzerland) · 2026Article
- Inhibition of STING pathway attenuates experimental abdominal aortic aneurysm progression.Acta pharmacologica Sinica · 2026Article
- Identification of human MLKL Cys184 and HSPBP1 Cys201 as novel cellular targets for necroptosis.Cell death & disease · 2026Article
- The RIPK3-IL-6 axis mediates kidney injury in cytokine storm syndrome.Cell death & disease · 2026Article
- Ferroptosis of smooth muscle cells in vascular diseases: from basic principles to clinical translation.Cell death discovery · 2026Review
- Loss of MLKL impairs abdominal aortic aneurysm development by attenuating smooth muscle cell necroptosis.Cell death & disease · 2026Article
- Deficiency of p27Journal of vascular research · 2026Article
- Targeting Gut Microbiota to Combat Vascular Aging and Cardiovascular Disease: Mechanisms and Therapeutic Potential.Nutrients · 2025Review
- Recent Advances in Nanomedicine-Mediated Abdominal Aortic Aneurysm Treatment.Small methods · 2025Review
- Impact of the Transforming Growth Factor β (TGF-β) on Brain Aneurysm Formation and Development: A Literature Review.Cellular and molecular neurobiology · 2025Review
- The Role of Post-Translational Modifications in Necroptosis.Biomolecules · 2025Review
- Regulated vascular smooth muscle cell death in vascular diseases.Cell proliferation · 2024Review
- Mendelian randomization demonstrates a causal link between peripheral circulating acylcarnitines and intracranial aneurysms.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2024Article
- Macrophage-mediated downregulation of lncRNA Carmn in mouse abdominal aortic aneurysm.Vascular pharmacology · 2024Article
- Aortic aneurysms: current pathogenesis and therapeutic targets.Experimental & molecular medicine · 2023Review
- PKCδ regulates the vascular biology in diabetic atherosclerosis.Cell communication and signaling : CCS · 2023Review
- Comprehensive analysis of mitochondrial dysfunction and necroptosis in intracranial aneurysms from the perspective of predictive, preventative, and personalized medicine.Apoptosis : an international journal on programmed cell death · 2023Article
- Role of RIPK3‑CaMKII‑mPTP signaling pathway‑mediated necroptosis in cardiovascular diseases (Review).International journal of molecular medicine · 2023Review
- METTL3-METTL14 complex induces necroptosis and inflammation of vascular smooth muscle cells via promoting N6 methyladenosine mRNA methylation of receptor-interacting protein 3 in abdominal aortic aneurysms.Journal of cell communication and signaling · 2023Article
- Novel pharmacological approaches in abdominal aortic aneurysm.Clinical science (London, England : 1979) · 2023Review
22 more citing papers are in PubMed but not listed here.
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Authors and funding
6 authors at 1 institution in 2 countries.
Funding
Abstract
rationaleDepletion of medial smooth muscle cell (SMC) is a major pathological characteristic of abdominal aortic aneurysm (AAA), although the mechanism by which these cells are eliminated remains incompletely understood. We reasoned that necroptosis, a recently described form of necrosis mediated by receptor-interacting protein kinase 3 (RIP3), may contribute to AAA pathology through the induction of SMC death and the significant production of inflammatory cytokines.
objectiveTo test the hypothesis that RIP3-mediated necroptosis is actively involved in aneurysm pathogenesis. METHODS AND
resultsRIP3 and RIP1 levels were found to be elevated in human AAAs, most noticeably in SMCs. Elevations of RIP3 and SMC necrosis were also observed in the elastase-induced mouse model of AAAs. Deletion of one or both copies of Rip3 prevented AAA formation. By transplanting Rip3(+/-) aortae to Rip3(+/+) mice, we demonstrated that reduced Rip3 expression in arterial wall was the primary cause of aneurysm resistance. In vitro, adenoviral overexpression of RIP3 was sufficient to trigger SMC necroptosis. Protein kinase C-delta contributed to tumor necrosis factor-α-induced SMC necroptosis by regulating Rip3 expression. Furthermore, Rip3 deficiency impaired tumor necrosis factor-α-induced inflammatory gene expression in aortic SMCs, which was at least in part because of attenuation of p65 Ser536 phosphorylation. In vivo, the lack of RIP3 diminished activation of p65 in SMCs, implicating a necrosis independent function of RIP3 in aneurysms.
conclusionsEnhanced RIP3 signaling in aneurysmal tissues contributes to AAA progression by causing SMC necroptosis, as well as stimulating vascular inflammation, and therefore may serve as a novel therapeutic target for AAA treatment.
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