ArticleCardiovascular research2015
Cardioprotection by H2S engages a cGMP-dependent protein kinase G/phospholamban pathway.
Article in Cardiovascular research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 2 of them syntheses that pooled it.
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Who cites it
36 citing papers in PubMed, 2 syntheses or guidelines pooled it, 80 citations in OpenAlex.
- Practical guidelines for rigor and reproducibility in preclinical and clinical studies on cardioprotection.Basic research in cardiology · 2018Guideline
- Pre- and postconditioning the heart with hydrogen sulfide (HBasic research in cardiology · 2018Pooled it
- Hydrogen Sulfide: A Versatile Molecule and Therapeutic Target in Health and Diseases.Biomolecules · 2024Review
- Role of hydrogen sulfide in health and disease.MedComm · 2024Review
- Review
- A novel role for phospholamban in the thalamic reticular nucleus.Scientific reports · 2024Article
- Using mechanism-based combinations of HNaunyn-Schmiedeberg's archives of pharmacology · 2024Article
- Health position paper and redox perspectives on reactive oxygen species as signals and targets of cardioprotection.Redox biology · 2023Review
- Sodium Thiosulfate in Acute Myocardial Infarction: A Randomized Clinical Trial.JACC. Basic to translational science · 2023Article
- CTH/MPST double ablation results in enhanced vasorelaxation and reduced blood pressureFrontiers in pharmacology · 2023Article
- Article
- Bibliometric evaluation of 2011-2021 publications on hydrogen sulfide in heart preservation research.Frontiers in cardiovascular medicine · 2022Article
- Modulation of EndMT by Hydrogen Sulfide in the Prevention of Cardiovascular Fibrosis.Antioxidants (Basel, Switzerland) · 2021Review
- HPharmacological research · 2020Review
- The role of mitochondrial reactive oxygen species, NO and HJournal of cellular and molecular medicine · 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 as a Potential Alternative for the Treatment of Myocardial Fibrosis.Oxidative medicine and cellular longevity · 2020Review
- Hydrogen sulfide-mediated endothelial function and the interaction with eNOS and PDE5A activity in human internal mammary arteries.The Journal of international medical research · 2019Article
- Hydrogen sulfide: a gaseous signaling molecule modulates tissue homeostasis: implications in ophthalmic diseases.Cell death & disease · 2019Review
- Nitroglycerine limits infarct size through S-nitrosation of cyclophilin D: a novel mechanism for an old drug.Cardiovascular research · 2019Article
Corrections and comments
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Authors and funding
12 authors at 8 institutions in 3 countries.
Funding
Abstract
aimsH2S is known to confer cardioprotection; however, the pathways mediating its effects in vivo remain incompletely understood. The purpose of the present study is to evaluate the contribution of cGMP-regulated pathways in the infarct-limiting effect of H2S in vivo. METHODS AND
resultsAnaesthetized rabbits were subjected to myocardial ischaemia (I)/reperfusion (R), and infarct size was determined in control or H2S-exposed groups. The H2S donor sodium hydrosulfide (NaHS, an agent that generates H2S) increased cardiac cGMP and reduced the infarct size. The cGMP-dependent protein kinase (PKG)-I inhibitor DT2 abrogated the protective effect of NaHS, whereas the control peptide TAT or l-nitroarginine methyl ester (l-NAME) did not alter the effect of NaHS. Moreover, the KATP channel inhibitor, glibenclamide, partially reversed the effects of NaHS, whereas inhibition of mitochondrial KATP did not modify the NaHS response. NaHS enhanced phosphorylation of phospholamban (PLN), in a PKG-dependent manner. To further investigate the role of PLN in H2S-mediated cardioprotection, wild-type and PLN KO mice underwent I/R. NaHS did not exert cardioprotection in PLN KO mice. Unlike what was observed in rabbits, genetic or pharmacological inhibition of eNOS abolished the infarct-limiting effect of NaHS in mice.
conclusionsOur findings demonstrate (i) that administration of NaHS induces cardioprotection via a cGMP/PKG/PLN pathway and (ii) contribution of nitric oxide to the H2S response is species-specific.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.