ArticleRedox biology2020
Keap1 controls protein S-nitrosation and apoptosis-senescence switch in endothelial cells.
Article in Redox biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
16 citing papers in PubMed, 32 citations in OpenAlex.
- Melatonin ameliorates circadian rhythm disruption induced erectile dysfunction by inhibiting oxidative stress mediated pyroptosis via Nrf2/HO‑1 axis.International journal of molecular medicine · 2026Article
- Tooth Decay Promotes Senescence in Dental Pulp Stem Cells, Modifying Their Biological and Proteomic Profiles.Journal of cellular physiology · 2026Article
- [Human umbilical cord mesenchymal stem cells protect against neonatal white matter injury by activating the Nrf2/Keap1/HO-1 signaling pathway].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2025Article
- Relationship between plasma homocysteine and clinical grading of varicocele.Asian journal of andrology · 2025Article
- New insights into crosstalk between Nrf2 pathway and ferroptosis in lung disease.Cell death & disease · 2024Review
- Advances in Understanding the Role of NRF2 in Liver Pathophysiology and Its Relationship with Hepatic-Specific Cyclooxygenase-2 Expression.Antioxidants (Basel, Switzerland) · 2023Review
- Dexmedetomidine attenuates airway inflammation and oxidative stress in asthma via the Nrf2 signaling pathway.Molecular medicine reports · 2023Article
- Mechanism of homocysteine-mediated endothelial injury and its consequences for atherosclerosis.Frontiers in cardiovascular medicine · 2022Review
- Contributions of Costimulatory Molecule CD137 in Endothelial Cells.Journal of the American Heart Association · 2021Review
- Bioactive Peptide F2d Isolated from Rice Residue Exerts Antioxidant Effects via Nrf2 Signaling Pathway.Oxidative medicine and cellular longevity · 2021Article
- UBE2E3 regulates cellular senescence and osteogenic differentiation of BMSCs during aging.PeerJ · 2021Article
- p53 SUMOylation Mediates AOPP-Induced Endothelial Senescence and Apoptosis Evasion.Frontiers in cardiovascular medicine · 2021Article
- Role of Nrf2 in cell senescence regulation.Molecular and cellular biochemistry · 2021Review
- Beyond repression of Nrf2: An update on Keap1.Free radical biology & medicine · 2020Review
- Keap1 governs ageing-induced protein aggregation in endothelial cells.Redox biology · 2020Article
- Simvastatin Attenuates Abdominal Aortic Aneurysm Formation Favoured by Lack of Nrf2 Transcriptional Activity.Oxidative medicine and cellular longevity · 2020Article
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 2 countries.
Funding
Abstract
Premature senescence, a death escaping pathway for cells experiencing stress, is conducive to aging and cardiovascular diseases. The molecular switch between senescent and apoptotic fate remains, however, poorly recognized. Nrf2 is an important transcription factor orchestrating adaptive response to cellular stress. Here, we show that both human primary endothelial cells (ECs) and murine aortas lacking Nrf2 signaling are senescent but unexpectedly do not encounter damaging oxidative stress. Instead, they exhibit markedly increased S-nitrosation of proteins. A functional role of S-nitrosation is protection of ECs from death by inhibition of NOX4-mediated oxidative damage and redirection of ECs to premature senescence. S-nitrosation and senescence are mediated by Keap1, a direct binding partner of Nrf2, which colocalizes and precipitates with nitric oxide synthase (NOS) and transnitrosating protein GAPDH in ECs devoid of Nrf2. We conclude that the overabundance of this "unrestrained" Keap1 determines the fate of ECs by regulation of S-nitrosation and propose that Keap1/GAPDH/NOS complex may serve as an enzymatic machinery for S-nitrosation in mammalian cells.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.