ArticleBritish journal of pharmacology2018
Hydrogen sulfide pretreatment improves mitochondrial function in myocardial hypertrophy via a SIRT3-dependent manner.
Article in British journal of pharmacology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.
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Who cites it
61 citing papers in PubMed, 124 citations in OpenAlex.
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- MARCH5 Promotes Cardiac Hypertrophy by Regulating Akt/mTOR/Gsk-3β/GATA4 Signalling Pathway.Journal of cellular and molecular medicine · 2025Article
- Cell migration in diabetic wound healing: Molecular mechanisms and therapeutic strategies (Review).International journal of molecular medicine · 2025Review
- Au@Pt Nanoparticles Enhance Maturation and Contraction of Mouse Embryonic Stem Cells-Derived and Neonatal Mouse Cardiomyocytes.Tissue engineering and regenerative medicine · 2025Article
- Impaired Iron-Sulfur Cluster Synthesis Induces Mitochondrial PARthanatos in Diabetic Cardiomyopathy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Pharmacological potential of Chinese botanical drugs in managing chronic kidney disease by targeting mitochondrial quality control.Frontiers in pharmacology · 2025Review
- The functional role of m6A demethylase ALKBH5 in cardiomyocyte hypertrophy.Cell death & disease · 2024Article
- Cytoplasmic Escape of Mitochondrial DNA Mediated by Mfn2 Downregulation Promotes Microglial Activation via cGas-Sting Axis in Spinal Cord Injury.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- The Regulatory Effect of Receptor-Interacting Protein Kinase 3 on CaMKIIδ in TAC-Induced Myocardial Hypertrophy.International journal of molecular sciences · 2023Article
- Dihydromyricetin Attenuates Diabetic Cardiomyopathy by Inhibiting Oxidative Stress, Inflammation and Necroptosis via Sirtuin 3 Activation.Antioxidants (Basel, Switzerland) · 2023Article
- A novel mechanism for the protection against acute lung injury by melatonin: mitochondrial quality control of lung epithelial cells is preserved through SIRT3-dependent deacetylation of SOD2.Cellular and molecular life sciences : CMLS · 2022Article
- The role of Mitochondrial Fission Proteins in Mitochondrial Dynamics in Kidney Disease.International journal of molecular sciences · 2022Review
- Hydrogen Sulfide Biomedical Research in China-20 Years of Hindsight.Antioxidants (Basel, Switzerland) · 2022Review
- Sodium Thiosulphate-Loaded Liposomes Control Hydrogen Sulphide Release and Retain Its Biological Properties in Hypoxia-like Environment.Antioxidants (Basel, Switzerland) · 2022Article
- The Mfn1-βIIPKC Interaction Regulates Mitochondrial Dysfunction via Sirt3 Following Experimental Subarachnoid Hemorrhage.Translational stroke research · 2022Article
- Review
- Mitochondrial-Targeted Therapies Require Mitophagy to Prevent Oxidative Stress Induced by SOD2 Inactivation in Hypertrophied Cardiomyocytes.Antioxidants (Basel, Switzerland) · 2022Article
- Sirtuin 3 Dependent and Independent Effects of NADAntioxidants (Basel, Switzerland) · 2022Article
- Sirt3, 6, and 7 Genes Expression in Gastric Antral Epithelial Cells of Patients with Helicobacter pylori Infection.Current microbiology · 2022Article
- Article
1 more citing papers are in PubMed but not listed here.
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
background and purposeHydrogen sulfide (H EXPERIMENTAL APPROACH: Neonatal rat cardiomyocytes were pretreated with NaHS (50 μM) for 4 h followed by angiotensin II (Ang II, 100 nM) for 24 h. SIRT3 was silenced with siRNA technology. SIRT3 promoter activity and expression, cell surface, hypertrophic gene mRNA expression, mitochondrial oxygen consumption rate and membrane potential were measured. Male 129S1/SvImJ [wild-type (WT)] and SIRT3 knockout (KO) mice were injected with NaHS (50 μmol·kg KEY
resultsIn vitro, NaHS increased SIRT3 promoter activity and SIRT3 expression in Ang II-induced cardiomyocyte hypertrophy. SIRT3 silencing abolished the ability of NaHS to reverse the Ang II-induced cardiomyocyte hypertrophy, mitochondrial function impairment and permeability potential dysfunction, along with the decline in FOXO3a and SOD2 expression. In vivo, after TAC. NaHS attenuated myocardial hypertrophy, inhibited oxidative stress, improved mitochondrial ultrastructure, suppressed mitochondrial volume but increased mitochondrial numbers, enhanced OPA1, MFN1 and MFN2 expression but suppressed DRP1 and FIS1 expression in WT mice but not in SIRT3 KO mice CONCLUSION AND IMPLICATIONS: NaHS improved mitochondrial function and inhibited oxidative stress in myocardial hypertrophy in a SIRT3-dependent manner. LINKED ARTICLES: This article is part of a themed section on Spotlight on Small Molecules in Cardiovascular Diseases. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v175.8/issuetoc.
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