ArticleCirculation. Heart failure2016
Sodium Sulfide Attenuates Ischemic-Induced Heart Failure by Enhancing Proteasomal Function in an Nrf2-Dependent Manner.
Article in Circulation. Heart failure, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.
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Who cites it
35 citing papers in PubMed, 1 synthesis or guideline pooled it, 67 citations in OpenAlex.
- Guidelines for in vivo mouse models of myocardial infarction.American journal of physiology. Heart and circulatory physiology · 2021Guideline
- Novel Allogeneic Mitochondria and Associated Organelle Complex Treatment Prevents Myocardial Ischemia-Reperfusion Injury Through Anti-Apoptotic Effects.JACC. Asia · 2026Article
- Intersection of HNeurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025Review
- NRF2 activation in the heart induces glucose metabolic reprogramming and reduces cardiac dysfunction via upregulation of the pentose phosphate pathway.Cardiovascular research · 2025Article
- Hydrogen Sulfide and Irisin, Potential Allies in Ensuring Cardiovascular Health.Antioxidants (Basel, Switzerland) · 2024Review
- Interactions Between the Ubiquitin-Proteasome System, Nrf2, and the Cannabinoidome as Protective Strategies to Combat Neurodegeneration: Review on Experimental Evidence.Neurotoxicity research · 2024Review
- Review
- Cardiac Lymphatic Insufficiency Leads to Diastolic Dysfunction Via Myocardial Morphologic Change.JACC. Basic to translational science · 2023Article
- Hydrogen sulfide donor activates AKT-eNOS signaling and promotes lymphatic vessel formation.PloS one · 2023Article
- Hydrogen Sulfide Attenuates Lymphedema Via the Induction of Lymphangiogenesis Through a PI3K/Akt-Dependent Mechanism.Journal of the American Heart Association · 2022Article
- Intersection of the Ubiquitin-Proteasome System with Oxidative Stress in Cardiovascular Disease.International journal of molecular sciences · 2022Review
- Reduced Levels of HAntioxidants (Basel, Switzerland) · 2022Article
- DJ-1 attenuates the glycation of mitochondrial complex I and complex III in the post-ischemic heart.Scientific reports · 2021Article
- Nrf2 for cardiac protection: pharmacological options against oxidative stress.Trends in pharmacological sciences · 2021Review
- Spatiotemporal regulation of hydrogen sulfide signaling in the kidney.Redox biology · 2021Review
- Modulation of EndMT by Hydrogen Sulfide in the Prevention of Cardiovascular Fibrosis.Antioxidants (Basel, Switzerland) · 2021Review
- NRF2 in Cardiovascular Diseases: a Ray of Hope!Journal of cardiovascular translational research · 2021Review
- Hydrogen sulfide restores cardioprotective effects of remote ischemic preconditioning in aged ratsThe Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2021Article
- Hydrogen Sulfide as a Potential Therapy for Heart Failure-Past, Present, and Future.Antioxidants (Basel, Switzerland) · 2021Review
- Harnessing the Benefits of Endogenous Hydrogen Sulfide to Reduce Cardiovascular Disease.Antioxidants (Basel, Switzerland) · 2021Review
Corrections and comments
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
Abstract
backgroundTherapeutic strategies aimed at increasing hydrogen sulfide (H2S) levels exert cytoprotective effects in various models of cardiovascular injury. However, the underlying mechanism(s) responsible for this protection remain to be fully elucidated. Nuclear factor E2-related factor 2 (Nrf2) is a cellular target of H2S and facilitator of H2S-mediated cardioprotection after acute myocardial infarction. Here, we tested the hypothesis that Nrf2 mediates the cardioprotective effects of H2S therapy in the setting of heart failure. METHODS AND
resultsMice (12 weeks of age) deficient in Nrf2 (Nrf2 KO; C57BL/6J background) and wild-type littermates were subjected to ischemic-induced heart failure. Wild-type mice treated with H2S in the form of sodium sulfide (Na2S) displayed enhanced Nrf2 signaling, improved left ventricular function, and less cardiac hypertrophy after the induction of heart failure. In contrast, Na2S therapy failed to provide protection against heart failure in Nrf2 KO mice. Studies aimed at evaluating the underlying cardioprotective mechanisms found that Na2S increased the expression of proteasome subunits, resulting in an increased proteasome activity and a reduction in the accumulation of damaged proteins. In contrast, Na2S therapy failed to enhance the proteasome and failed to attenuate the accumulation of damaged proteins in Nrf2 KO mice. Additionally, Na2S failed to improve cardiac function when the proteasome was inhibited.
conclusionsThese findings indicate that Na2S therapy enhances proteasomal activity and function during the development of heart failure in an Nrf2-dependent manner and that this enhancement leads to attenuation in cardiac dysfunction.
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