ArticleRedox biology2018
GSNOR modulates hyperhomocysteinemia-induced T cell activation and atherosclerosis by switching Akt S-nitrosylation to phosphorylation.
Article in Redox biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed.
- Fenofibrate attenuates hyperhomocysteinemia-potentiated thrombosis by restoring platelet fatty acid β-oxidation.Redox biology · 2026Article
- Role of hyperhomocysteinemia in atherosclerosis: from bench to bedside.Annals of medicine · 2025Review
- Nitric oxide‑mediated S‑Nitrosylation contributes to signaling transduction in human physiological and pathological status (Review).International journal of molecular medicine · 2025Review
- S-Nitrosylation: Mechanistic Links between Nitric Oxide Signaling and Atherosclerosis.Current atherosclerosis reports · 2025Review
- S-Nitrosylation in Cardiovascular Disorders: The State of the Art.Biomolecules · 2025Review
- Role of DZ2002 in reducing corneal graft rejection in rats by influencing Th17 activation via inhibition of the PI3K/AKT pathway and downregulation of TRAF1.Open life sciences · 2025Article
- GSNOR overexpression enhances CAR-T cell stemness and anti-tumor function by enforcing mitochondrial fitness.Molecular therapy : the journal of the American Society of Gene Therapy · 2024Article
- Facilitating Nitrite-Derived S-Nitrosothiol Formation in the Upper Gastrointestinal Tract in the Therapy of Cardiovascular Diseases.Antioxidants (Basel, Switzerland) · 2024Review
- GSNOR negatively regulates the NLRP3 inflammasome via S-nitrosation of MAPK14.Cellular & molecular immunology · 2024Article
- Primary and Secondary Coordination Sphere Effects on the Structure and Function ofJournal of the American Chemical Society · 2023Article
- Roles of protein post-translational modifications in glucose and lipid metabolism: mechanisms and perspectives.Molecular medicine (Cambridge, Mass.) · 2023Review
- Selected Biomarkers of Oxidative Stress and Energy Metabolism Disorders in Neurological Diseases.Molecular neurobiology · 2023Review
- GSNOR facilitates antiviral innate immunity by restricting TBK1 cysteine S-nitrosation.Redox biology · 2021Article
- S-nitrosylation-mediated coupling of G-protein alpha-2 with CXCR5 induces Hippo/YAP-dependent diabetes-accelerated atherosclerosis.Nature communications · 2021Article
- S-Nitrosylation in Tumor Microenvironment.International journal of molecular sciences · 2021Review
- Nitric Oxide and Electrophilic Cyclopentenone Prostaglandins in Redox signaling, Regulation of Cytoskeleton Dynamics and Intercellular Communication.Frontiers in cell and developmental biology · 2021Review
- The Relationship Between Protein S-Nitrosylation and Human Diseases: A Review.Neurochemical research · 2020Review
- Post-Translational S-Nitrosylation of Proteins in Regulating Cardiac Oxidative Stress.Antioxidants (Basel, Switzerland) · 2020Review
- Herpud1 deficiency could reduce amyloid-β40 expression and thereby suppress homocysteine-induced atherosclerosis by blocking the JNK/AP1 pathway.Journal of physiology and biochemistry · 2020Article
- Abnormal Homocysteine Metabolism: An Insight of Alzheimer's Disease from DNA Methylation.Behavioural neurology · 2020Review
Corrections and comments
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Authors and funding
17 authors.
Funding
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Abstract
The adaptive immune system plays a critical role in hyperhomocysteinemia (HHcy)-accelerated atherosclerosis. Recent studies suggest that HHcy aggravates atherosclerosis with elevated oxidative stress and reduced S-nitrosylation level of redox-sensitive protein residues in the vasculature. However, whether and how S-nitrosylation contributes to T-cell-driven atherosclerosis remain unclear. In the present study, we report that HHcy reduced the level of protein S-nitrosylation in T cells by inducing S-nitrosoglutathione reductase (GSNOR), the key denitrosylase that catalyzes S-nitrosoglutathione (GSNO), which is the main restored form of nitric oxide in vivo. Consequently, secretion of inflammatory cytokines [interferon-γ (IFN-γ) and interleukin-2] and proliferation of T cells were increased. GSNOR knockout or GSNO stimulation rectified HHcy-induced inflammatory cytokine secretion and T-cell proliferation. Site-directed mutagenesis of Akt at Cys224 revealed that S-nitrosylation at this site was pivotal for the reduced phosphorylation at Akt Ser473, which led to impaired Akt signaling. Furthermore, on HHcy challenge, as compared with GSNOR
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