ArticleOxidative medicine and cellular longevity2016
The H2S Donor NaHS Changes the Expression Pattern of H2S-Producing Enzymes after Myocardial Infarction.
Article in Oxidative medicine and cellular longevity, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 45 citations in OpenAlex.
- Allicin ameliorates acute myocardial infarction in rats by modulating calcium homeostasis in cardiomyocytes through the induction of hydrogen sulfide production.Frontiers in pharmacology · 2025Article
- The effect of zofenopril on the cardiovascular system of spontaneously hypertensive rats treated with the ACE2 inhibitor MLN-4760.Biological research · 2023Article
- Recent advances in the role of endogenous hydrogen sulphide in cancer cells.Cell proliferation · 2023Review
- Role of 3-Mercaptopyruvate Sulfurtransferase (3-MST) in Physiology and Disease.Antioxidants (Basel, Switzerland) · 2023Review
- Article
- Hydrogen Sulfide Inhibited Sympathetic Activation in D-Galactose-Induced Aging Rats by Upregulating Klotho and Inhibiting Inflammation in the Paraventricular Nucleus.Biomedicines · 2023Article
- Function of gaseous hydrogen sulfide in liver fibrosis.BMB reports · 2022Review
- Hydrogen Sulfide Inhibits Ferroptosis in Cardiomyocytes to Protect Cardiac Function in Aging Rats.Frontiers in molecular biosciences · 2022Article
- HBiomolecules · 2021Review
- Trends in HAntioxidants (Basel, Switzerland) · 2021Review
- Point-of-care testing and optimization of sample treatment for fluorometric determination of hydrogen sulphide in plasma of cardiovascular patients.Journal of advanced research · 2021Review
- Norswertianolin Promotes Cystathionine γ-Lyase Activity and Attenuates Renal Ischemia/Reperfusion Injury and Hypertension.Frontiers in pharmacology · 2021Article
- Cardiac Protection by Oral Sodium Thiosulfate in a Rat Model of L-NNA-Induced Heart Disease.Frontiers in pharmacology · 2021Article
- Hydrogen sulfide, oxygen, and calcium regulation in developing human airway smooth muscle.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- Review
- Dose-Dependent Effects of Long-Term Administration of Hydrogen Sulfide on Myocardial Ischemia-Reperfusion Injury in Male Wistar Rats: Modulation of RKIP, NF-κB, and Oxidative Stress.International journal of molecular sciences · 2020Article
- From primordial gas to the medicine cabinet.British journal of pharmacology · 2020Article
- HJournal of experimental & clinical cancer research : CR · 2019Article
- Mechanisms by which hydrogen sulfide attenuates muscle function following ischemia-reperfusion injury: effects on Akt signaling, mitochondrial function, and apoptosis.Journal of translational medicine · 2019Review
- Endogenous CSE/Hydrogen Sulfide System Regulates the Effects of Glucocorticoids and Insulin on Muscle Protein Synthesis.Oxidative medicine and cellular longevity · 2019Article
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aims. To examine the expression patterns of hydrogen sulphide- (H2S-) producing enzymes in ischaemic heart tissue and plasma levels of H2S after 2 weeks of NaHS treatment after myocardial infarction (MI) and to clarify the role of endogenous H2S in the MI process. Results. After MI surgery, 2 weeks of treatment with the H2S donor NaHS alleviated ischaemic injury. Meanwhile, in ischemia myocardium, three H2S-producing enzymes, cystathionine γ-lyase (CSE), cystathionine-β-synthase (CBS), and 3-mercaptopyruvate sulfurtransferase (3-MST) significantly increased. Plasma H2S levels were also elevated. In vitro, NaHS treatment protected cardiomyocytes from hypoxic injury and raised CBS levels in a concentration-dependent manner. Different from in vivo results, however, CSE or 3-MST expression did not change. NaHS treatment increased the activity of CSE/CBS but not of 3-MST. When CSE was either knocked down (in vitro) or knocked out (in vivo), H2S levels significantly decreased, which subsequently exacerbated the ischaemic injury. Meanwhile, the expressions of CBS and 3-MST increased due to compensation. Conclusions. Exogenous H2S treatment changed the expressions of three H2S-producing enzymes and H2S levels after MI, suggesting a new and indirect regulatory mechanism for H2S production and its contribution to cardiac protection. Endogenous H2S plays an important role in protecting ischaemic tissue after MI.
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