ArticleScientific reports2017
Inhibition of Receptor-Interacting Protein Kinase 1 with Necrostatin-1s ameliorates disease progression in elastase-induced mouse abdominal aortic aneurysm model.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 53 citations in OpenAlex.
- Metabolic dysfunction-associated steatotic liver disease: pathogenic mechanisms and exercise-induced molecular adaptations.Lipids in health and disease · 2026Review
- Endothelial Integrin-Linked Kinase (ILK) Deficiency Promotes Endothelial Activation and Cardiovascular Dysfunction via Receptor Interacting Protein Kinase-1 (RIPK1) Enriched-Extracellular Vesicle Signalling.Journal of extracellular vesicles · 2026Article
- Loss of MLKL impairs abdominal aortic aneurysm development by attenuating smooth muscle cell necroptosis.Cell death & disease · 2026Article
- Regulated vascular smooth muscle cell death in vascular diseases.Cell proliferation · 2024Review
- Necroptosis inhibitors: mechanisms of action and therapeutic potential.Apoptosis : an international journal on programmed cell death · 2024Review
- Role of RIPK3‑CaMKII‑mPTP signaling pathway‑mediated necroptosis in cardiovascular diseases (Review).International journal of molecular medicine · 2023Review
- Nephropathy Is Aggravated by Fatty Acids in Diabetic Kidney Disease through Tubular Epithelial Cell Necroptosis and Is Alleviated by an RIPK-1 Inhibitor.Kidney diseases (Basel, Switzerland) · 2023Article
- 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
- Endothelial RIPK1 protects artery bypass graft against arteriosclerosis by regulating SMC growth.Science advances · 2023Article
- HMGB1/TLR4 signaling pathway enhances abdominal aortic aneurysm progression in mice by upregulating necroptosis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023Article
- Programmed cell death in aortic aneurysm and dissection: A potential therapeutic target.Journal of molecular and cellular cardiology · 2022Review
- Advances in RIPK1 kinase inhibitors.Frontiers in pharmacology · 2022Review
- Role of Necroptosis and Immune Infiltration in Human Stanford Type A Aortic Dissection: Novel Insights from Bioinformatics Analyses.Oxidative medicine and cellular longevity · 2022Article
- Vascular Smooth Muscle Cells in Aortic Aneurysm: From Genetics to Mechanisms.Journal of the American Heart Association · 2021Article
- The role of necroptosis in disease and treatment.MedComm · 2021Review
- Article
- PLK1-mediated S369 phosphorylation of RIPK3 during G2 and M phases enables its ripoptosome incorporation and activity.iScience · 2021Article
- Macrophage Biology in Cardiovascular Diseases.Arteriosclerosis, thrombosis, and vascular biology · 2021Review
- Necrostatin-1 and necroptosis inhibition: Pathophysiology and therapeutic implications.Pharmacological research · 2021Review
- Receptor Interacting Protein Kinases 1/3: The Potential Therapeutic Target for Cardiovascular Inflammatory Diseases.Frontiers in pharmacology · 2021Review
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 2 countries.
Funding
Abstract
Abdominal aortic aneurysm (AAA) is a common aortic disease with a progressive nature. There is no approved pharmacological treatment to effectively slow aneurysm growth or prevent rupture. Necroptosis is a form of programmed necrosis that is regulated by receptor-interacting protein kinases (RIPs). We have recently demonstrated that the lack of RIP3 in mice prevented aneurysm formation. The goal of the current study is to test whether perturbing necroptosis affects progression of existing aneurysm using the RIP1 inhibitors Necrostatin-1 (Nec-1) and an optimized form of Nec-1, 7-Cl-O-Nec-1 (Nec-1s). Seven days after aneurysm induction by elastase perfusion, mice were randomly administered DMSO, Nec-1 (3.2 mg/kg/day) and Nec-1s (1.6 mg/kg/day) via intraperitoneal injection. Upon sacrifice on day 14 postaneurysm induction, the aortic expansion in the Nec-1s group (64.12 ± 4.80%) was significantly smaller than that of the DMSO group (172.80 ± 13.68%) (P < 0.05). The mean aortic diameter of Nec-1 treated mice appeared to be smaller (121.60 ± 10.40%) than the DMSO group, though the difference was not statistically significant (P = 0.1). Histologically, the aortic structure of Nec-1s-treated mice appeared normal, with continuous and organized elastin laminae and abundant αActin-expressing SMCs. Moreover, Nect-1s treatment diminished macrophage infiltration and MMP9 accumulation and increased aortic levels of tropoelastin and lysyl oxidase. Together, our data suggest that pharmacological inhibition of necroptosis with Nec-1s stabilizes pre-existing aneurysms by diminishing inflammation and promoting connective tissue repair.
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