ArticleMedical gas research2014
Hydrogen sulfide provides cardioprotection against myocardial/ischemia reperfusion injury in the diabetic state through the activation of the RISK pathway.
Article in Medical gas research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.
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Who cites it
24 citing papers in PubMed, 1 synthesis or guideline pooled it, 43 citations in OpenAlex.
- Pre- and postconditioning the heart with hydrogen sulfide (HBasic research in cardiology · 2018Pooled it
- Hydrogen Sulfide in Experimental Organ Transplantation: From Bench to Bedside.Handbook of experimental pharmacology · 2026Review
- The role of ERK1/2 signaling in diabetes: pathogenic and therapeutic implications.Frontiers in pharmacology · 2025Review
- Signaling Paradigms of HAntioxidants (Basel, Switzerland) · 2024Review
- Using mechanism-based combinations of HNaunyn-Schmiedeberg's archives of pharmacology · 2024Article
- Article
- Preliminary evidence for the presence of multiple forms of cell death in diabetes cardiomyopathy.Acta pharmaceutica Sinica. B · 2022Review
- The prognostic implications of perioperative endogenous hydrogen sulfide and nitric oxide levels in children with congenital heart disease complicated by pulmonary arterial hypertension.European journal of pediatrics · 2021Article
- The Potential of Hydrogen Sulfide Donors in Treating Cardiovascular Diseases.International journal of molecular sciences · 2021Review
- An Updated Insight Into Molecular Mechanism of Hydrogen Sulfide in Cardiomyopathy and Myocardial Ischemia/Reperfusion Injury Under Diabetes.Frontiers in pharmacology · 2021Review
- Involvement of amylin B-H2S-connexin 43 signaling pathway in vascular dysfunction and enhanced ischemia-reperfusion-induced myocardial injury in diabetic rats.Bioscience reports · 2020Article
- Diabetic Cardiomyopathy and Ischemic Heart Disease: Prevention and Therapy by Exercise and Conditioning.International journal of molecular sciences · 2020Review
- Mitochondrial dysfunction plays a key role in the abrogation of cardioprotection by sodium hydrosulfide post-conditioning in diabetic cardiomyopathy rat heart.Naunyn-Schmiedeberg's archives of pharmacology · 2020Article
- Hydrogen sulfide-mediated regulation of cell death signaling ameliorates adverse cardiac remodeling and diabetic cardiomyopathy.American journal of physiology. Heart and circulatory physiology · 2019Review
- Diabetes abolish cardioprotective effects of remote ischemic conditioning: evidences and possible mechanisms.Journal of physiology and biochemistry · 2019Review
- DL-Propargylglycine protects against myocardial injury induced by chronic intermittent hypoxia through inhibition of endoplasmic reticulum stress.Sleep & breathing = Schlaf & Atmung · 2018Article
- Hyperhomocysteinemia potentiates diabetes-impaired EDHF-induced vascular relaxation: Role of insufficient hydrogen sulfide.Redox biology · 2018Article
- Essential role for EGFR tyrosine kinase and ER stress in myocardial infarction in type 2 diabetes.Pflugers Archiv : European journal of physiology · 2018Article
- Beyond a Gasotransmitter: Hydrogen Sulfide and Polysulfide in Cardiovascular Health and Immune Response.Antioxidants & redox signaling · 2017Review
- The Role of ERK1/2 in the Development of Diabetic Cardiomyopathy.International journal of molecular sciences · 2016Review
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5 authors at 1 institution in 1 country.
Funding
Abstract
backgroundCoronary artery disease remains the principal cause of death in patients with diabetes mellitus. Diabetic mice display exacerbated injury following myocardial ischemia-reperfusion (MI/R) and are resistant to most therapeutic interventions. We have reported that sodium sulfide (Na2S) therapy confers cardioprotection during MI/R in non-diabetic mice. Here we tested the hypothesis that Na2S therapy would limit the extent of myocardial injury following MI/R when administered at the time of reperfusion. METHODS AND
resultsDiabetic mice (db/db, 12 weeks of age) were subjected to transient myocardial ischemia for a period of 30 minutes followed by reperfusion up to 24 hours. Na2S (0.05 to 1 mg/kg) or saline (vehicle) was administered into the left ventricular lumen at the time of reperfusion. Na2S therapy significantly decreased myocardial injury in the db/db diabetic mouse, as evidenced by a reduction in infarct size and circulating troponin-I levels. The reduction in myocardial injury was also associated with a reduction in oxidative stress and a decrease in cleaved caspase-3 expression. In an effort to evaluate the signaling mechanism responsible for the observed cardioprotection, additional groups of mice were sacrificed during early reperfusion. Hearts were excised and processed for Western blot analysis. These studies revealed that Na2S therapy activated the Erk1/2 arm of the Reperfusion Injury Salvage Kinase (RISK) pathway.
conclusionThese findings provide important information that myocardial Erk1/2 activation by Na2S therapy following MI/R sets into motion events, which ultimately lead to cardioprotection in the setting of diabetes.
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