ArticleCirculation2019
Improvement in Outcomes After Cardiac Arrest and Resuscitation by Inhibition of S-Nitrosoglutathione Reductase.
Article in Circulation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 64 citations in OpenAlex.
- Blood Plasma's Protective Ability against the Degradation of S-Nitrosoglutathione under the Influence of Air-Pollution-Derived Metal Ions in Patients with Exacerbation of Heart Failure and Coronary Artery Disease.International journal of molecular sciences · 2021Trial
- Brain Hypoxia Is Associated With Neuroglial Injury in Humans Post-Cardiac Arrest.Circulation research · 2021Trial
- Protein S-nitrosylation in the heart: Mechanisms, physiological roles, and pathological remodeling.Redox biology · 2026Review
- GNPs-pIL-4 reprograms macrophage polarization and activates the OSM/GSNOR/ENG axis to improve angiogenesis in ischemic limbs.Science advances · 2026Article
- Nitric Oxide Donor Alleviates Cardiac Arrest Induced Blood Brain Barrier Injury by Inhibiting HMGB1-ATG5 Mediated Endothelial Autophagy.Cellular and molecular neurobiology · 2026Article
- S-nitrosoglutathione reductase GSNOR drives age-related obesity by promoting adipose tissue whitening through de-nitrosation of Beclin-1.Nature communications · 2026Article
- Systemic inflammatory response drives post-cardiac arrest multi-organ injury via IL-17 signaling in murine and porcine models.Frontiers in immunology · 2026Article
- Article
- Dysregulated ProteinCirculation research · 2025Article
- The denitrosylase SCoR2 controls cardioprotective metabolic reprogramming.bioRxiv : the preprint server for biology · 2025Article
- Proteomics identify pathogenesis and novel biomarkers for monitoring and early prognostication of brain injury after cardiac arrest: a randomized animal study.Resuscitation plus · 2025Article
- Systemic nicotinamide mononucleotide administration to mitigate post-cardiac arrest brain injury in mice.PloS one · 2025Article
- ADH5 inhibits proliferation but promotes EMT in non-small cell lung cancer cell through activating Smad2/Smad3.Open life sciences · 2025Article
- Hemoglobin vesicles improve neurological outcomes after cardiac arrest in rats.Resuscitation plus · 2024Article
- Carbon monoxide-releasing molecule-3 exerts neuroprotection effects after cardiac arrest in mice: A randomized controlled study.Resuscitation plus · 2024Article
- Neuroprotective Approaches for Brain Injury After Cardiac Arrest: Current Trends and Prospective Avenues.Journal of stroke · 2024Review
- Differences in Pathophysiology and Treatment Efficacy Based on Heterogeneous Out-of-Hospital Cardiac Arrest.Medicina (Kaunas, Lithuania) · 2024Review
- Indoleamine 2,3-Dioxygenase Deletion to Modulate Kynurenine Pathway and to Prevent Brain Injury after Cardiac Arrest in Mice.Anesthesiology · 2023Article
- Clinical targeting of the cerebral oxygen cascade to improve brain oxygenation in patients with hypoxic-ischaemic brain injury after cardiac arrest.Intensive care medicine · 2023Review
- Cathepsin B S-nitrosylation promotes ADAR1-mediated editing of its own mRNA transcript via an ADD1/MATR3 regulatory axis.Cell research · 2023Article
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Authors and funding
18 authors at 5 institutions in 1 country.
Funding
Abstract
backgroundThe biological effects of nitric oxide are mediated via protein S-nitrosylation. Levels of S-nitrosylated protein are controlled in part by the denitrosylase, S-nitrosoglutathione reductase (GSNOR). The objective of this study was to examine whether GSNOR inhibition improves outcomes after cardiac arrest and cardiopulmonary resuscitation (CA/CPR).
methodsAdult wild-type C57BL/6 and GSNOR-deleted (GSNOR
resultsGSNOR activity was increased in plasma and multiple organs of mice, including brain in particular. Levels of protein S-nitrosylation were decreased in the brain 6 hours after CA/CPR. Administration of SPL-334.1 attenuated the increase in GSNOR activity in brain, heart, liver, spleen, and plasma, and restored S-nitrosylated protein levels in the brain. Inhibition of GSNOR attenuated ischemic brain injury and improved survival in wild-type mice after CA/CPR (81.8% in SPL-334.1 versus 36.4% in placebo; log rank P=0.031). Similarly, GSNOR deletion prevented the reduction in the number of S-nitrosylated proteins in the brain, mitigated brain injury, and improved neurological recovery and survival after CA/CPR. Both GSNOR inhibition and deletion attenuated CA/CPR-induced disruption of blood brain barrier. Post-CA patients had higher plasma GSNOR activity than did preoperative cardiac surgery patients or healthy volunteers ( P<0.0001). Plasma GSNOR activity was positively correlated with initial lactate levels in postarrest patients (Spearman correlation coefficient=0.48; P=0.045).
conclusionsCA and CPR activated GSNOR and reduced the number of S-nitrosylated proteins in the brain. Pharmacological inhibition or genetic deletion of GSNOR prevented ischemic brain injury and improved survival rates by restoring S-nitrosylated protein levels in the brain after CA/CPR in mice. Our observations suggest that GSNOR is a novel biomarker of postarrest brain injury as well as a molecular target to improve outcomes after CA.
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