ArticleCirculation research2018
S-Nitrosoglutathione Reductase Is Essential for Protecting the Female Heart From Ischemia-Reperfusion Injury.
Article in Circulation research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 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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Who cites it
32 citing papers in PubMed, 56 citations in OpenAlex.
- Protein S-nitrosylation in the heart: Mechanisms, physiological roles, and pathological remodeling.Redox biology · 2026Review
- Mitochondrial vulnerability to aldehydic load and the role mitochondrial aldehyde dehydrogenases.Pharmacological research · 2026Review
- Left bundle branch vs biventricular pacing: mechanistic insights from a canine model.European heart journal · 2026Article
- GSNOR deletion differentially alters age-related cardiac function in a sex-dependent manner.American journal of physiology. Heart and circulatory physiology · 2026Article
- Formate Reduces Ischemic Injury in Female Hearts Lacking Alcohol Dehydrogenase 5.FASEB bioAdvances · 2025Article
- Identification of IL1R1 as a potential key PANoptosis-related gene in myocardial ischemia-reperfusion injury using machine learning.Scientific reports · 2025Article
- Dysregulated ProteinCirculation research · 2025Article
- The role of S-nitrosoglutathione reductase (GSNOR) in T cell-mediated immunopathology of experimental autoimmune encephalomyelitis (EAE).Neuroscience · 2025Article
- ADH5 inhibits proliferation but promotes EMT in non-small cell lung cancer cell through activating Smad2/Smad3.Open life sciences · 2025Article
- Sex-dependent phosphorylation of Argonaute 2 reduces the mitochondrial translocation of miR-181c and induces cardioprotection in females.Journal of molecular and cellular cardiology · 2024Article
- Reduced cardiac antioxidant defenses mediate increased susceptibility to workload-induced myocardial injury in males with genetic cardiomyopathy.Journal of molecular and cellular cardiology · 2024Article
- Sterile inflammation induces vasculopathy and chronic lung injury in murine sickle cell disease.Free radical biology & medicine · 2024Article
- Supersulfide catalysis for nitric oxide and aldehyde metabolism.Science advances · 2023Article
- Cadmium exposure induces a sex-dependent decline in left ventricular cardiac function.Life sciences · 2023Article
- Thioredoxin 1 promotes autophagy through transnitrosylation of Atg7 during myocardial ischemia.The Journal of clinical investigation · 2023Article
- Loss of cardiomyocyte CYB5R3 impairs redox equilibrium and causes sudden cardiac death.The Journal of clinical investigation · 2022Article
- East Asian variant aldehyde dehydrogenase type 2 genotype exacerbates ischemia/reperfusion injury with ST-elevation myocardial infarction in men: possible sex differences.Heart and vessels · 2022Article
- New Perspectives on Sex Steroid and Mineralocorticoid Receptor Signaling in Cardiac Ischemic Injury.Frontiers in physiology · 2022Review
- Increased protein S-nitrosylation in mitochondria: a key mechanism of exercise-induced cardioprotection.Basic research in cardiology · 2021Article
- The cellular function and molecular mechanism of formaldehyde in cardiovascular disease and heart development.Journal of cellular and molecular medicine · 2021Review
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
rationaleProtein S-nitros(yl)ation (SNO) has been implicated as an essential mediator of nitric oxide-dependent cardioprotection. Compared with males, female hearts exhibit higher baseline levels of protein SNO and associated with this, reduced susceptibility to myocardial ischemia-reperfusion injury. Female hearts also exhibit enhanced S-nitrosoglutathione reductase (GSNO-R) activity, which would typically favor decreased SNO levels as GSNO-R mediates SNO catabolism.
objectiveBecause female hearts exhibit higher SNO levels, we hypothesized that GSNO-R is an essential component of sex-dependent cardioprotection in females. METHODS AND
resultsMale and female wild-type mouse hearts were subjected to ex vivo ischemia-reperfusion injury with or without GSNO-R inhibition (N6022). Control female hearts exhibited enhanced functional recovery and decreased infarct size versus control males. Interestingly, GSNO-R inhibition reversed this sex disparity, significantly reducing injury in male hearts, and exacerbating injury in females. Similar results were obtained with male and female GSNO-R
conclusionsThese striking findings point to GSNO-R as a critical sex-dependent mediator of myocardial protein SNO and formaldehyde levels and further suggest that different therapeutic strategies may be required to combat ischemic heart disease in males and females.
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Registered trials
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