ArticleCardiovascular research2024
Ncf1 knockout in smooth muscle cells exacerbates angiotensin II-induced aortic aneurysm and dissection by activating the STING pathway.
Article in Cardiovascular research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.
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Who cites it
16 citing papers in PubMed, 1 synthesis or guideline pooled it, 13 citations in OpenAlex.
- Human Transcriptomic Meta-Analysis Identifies Immune-Redox Remodeling and Impaired Vascular Wall Homeostasis in Abdominal Aortic Aneurysm.International journal of molecular sciences · 2026Pooled it
- Intracranial aneurysms as a manifestation of premature vascular aging: Cellular senescence, inflammaging, and wall degeneration.Ageing research reviews · 2026Review
- Integrated Single-Cell and Spatial Analysis Reveals a Metabolic-Immune Axis Driving Aortic Dissection.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Erosion or Explosion: Integrated Single-Cell Transcriptomics Reveals Cellular Heterogeneity in Aortic Aneurysm and Dissection.Inflammation · 2026Article
- SLC1A5 prevents aortic aneurysm and dissection by glutaminolytic-epigenetic orchestration of vascular smooth muscle cell homeostasis.Nature communications · 2026Article
- Bioinformatics Analysis of Ferroptosis-Related Driver Genes in Stanford Type A Aortic Dissection.Current issues in molecular biology · 2026Article
- Study on the Role and Mechanism ofJournal of cardiovascular development and disease · 2026Article
- Article
- Systemic inflammatory and metabolic indexes for aortic dissection: a machine learning analysis.BMC cardiovascular disorders · 2025Article
- Gut microbiota-derived butyrate prevents aortic dissection via GPR41.Acta pharmacologica Sinica · 2025Article
- cGAS/STING signalling in macrophages aggravates obliterative bronchiolitis via an IFN-α-dependent mechanism after orthotopic tracheal transplantation in mice.Clinical and translational medicine · 2025Article
- Connecting intermediate phenotypes to disease using multi-omics in heart failure.Pacific Symposium on Biocomputing. Pacific Symposium on Biocomputing · 2025Article
- The interplay of ferroptosis and oxidative stress in the pathogenesis of aortic dissection.Frontiers in pharmacology · 2025Review
- Regulation of osteogenic differentiation in vascular smooth muscle cells under high-glucose condition.Frontiers in endocrinology · 2025Review
- Role of macrophages in aortic dissection pathogenesis: insights from preclinical studies to translational prospective.Science China. Life sciences · 2024Review
- Connecting intermediate phenotypes to disease using multi-omics in heart failure.medRxiv : the preprint server for health sciences · 2024Article
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
Abstract
aimsAortic aneurysm and dissection (AAD) is caused by the progressive loss of aortic smooth muscle cells (SMCs) and is associated with a high mortality rate. Identifying the mechanisms underlying SMC apoptosis is crucial for preventing AAD. Neutrophil cytoplasmic factor 1 (Ncf1) is essential in reactive oxygen species production and SMC apoptosis; Ncf1 absence leads to autoimmune diseases and chronic inflammation. Here, the role of Ncf1 in angiotensin II (Ang II)-induced AAD was investigated. METHODS AND
resultsNcf1 expression increased in injured SMCs. Bioinformatic analysis identified Ncf1 as a mediator of AAD-associated SMC damage. Ncf1 expression is positively correlated with DNA replication and repair in SMCs of AAD aortas. AAD incidence increased in Ang II-challenged Sm22CreNcf1fl mice. Transcriptomics showed that Ncf1 knockout activated the stimulator of interferon genes (STING) and cell death pathways. The effects of Ncf1 on SMC death and the STING pathway in vitro were examined. Ncf1 regulated the hydrogen peroxide-mediated activation of the STING pathway and inhibited SMC apoptosis. Mechanistically, Ncf1 knockout promoted the ubiquitination of nuclear factor erythroid 2-related factor 2 (NRF2), thereby inhibiting the negative regulatory effect of NRF2 on the stability of STING mRNA and ultimately promoting STING expression. Additionally, the pharmacological inhibition of STING activation prevented AAD progression.
conclusionNcf1 deficiency in SMCs exacerbated Ang II-induced AAD by promoting NRF2 ubiquitination and degradation and activating the STING pathway. These data suggest that Ncf1 may be a potential therapeutic target for AAD treatment.
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