ArticleThe American journal of pathology2011
The pathogenic role of cystathionine γ-lyase/hydrogen sulfide in streptozotocin-induced diabetes in mice.
Article in The American journal of pathology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.
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Who cites it
34 citing papers in PubMed, 1 synthesis or guideline pooled it, 76 citations in OpenAlex.
- Recent Advances in Molecular Research on Hydrogen Sulfide (HInternational journal of molecular sciences · 2022Pooled it
- The Role of Ferroptosis in Diabetes Pathogenesis: Therapeutic Implications of Hydrogen Sulfide and Its Reactive Metabolites.Antioxidants (Basel, Switzerland) · 2026Review
- Crosstalk Between HHandbook of experimental pharmacology · 2026Review
- Black gas, bright future: HNeurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025Review
- Dual Regulation of Mitochondrial Complexes by HBiomolecules · 2025Article
- Diabetic Nephropathy and Gaseous Modulators.Antioxidants (Basel, Switzerland) · 2023Review
- Reduced Levels of HAntioxidants (Basel, Switzerland) · 2022Article
- Effects of Sodium Thiosulfate During Resuscitation From Trauma-and-Hemorrhage in Cystathionine-γ-Lyase Knockout Mice With Diabetes Type 1.Frontiers in medicine · 2022Article
- The DR1‑CSE/HInternational journal of molecular medicine · 2022Article
- Exogenous Hydrogen Sulfide Plays an Important Role by Regulating Autophagy in Diabetic-Related Diseases.International journal of molecular sciences · 2021Review
- Hydrogen Sulfide and the Kidney.Advances in experimental medicine and biology · 2021Article
- The Role of HAdvances in experimental medicine and biology · 2021Article
- Hydrogen sulfide regulates insulin secretion and insulin resistance in diabetes mellitus, a new promising target for diabetes mellitus treatment? A review.Journal of advanced research · 2021Review
- Potential role of hydrogen sulfide in diabetes-impaired angiogenesis and ischemic tissue repair.Redox biology · 2020Review
- Diabetic nephropathy associates with deregulation of enzymes involved in kidney sulphur metabolism.Journal of cellular and molecular medicine · 2020Article
- Hydrogen Sulfide, Adipose Tissue and Diabetes Mellitus.Diabetes, metabolic syndrome and obesity : targets and therapy · 2020Review
- Hydrogen Sulfide in Renal Physiology and Disease.Antioxidants & redox signaling · 2016Review
- Decreased Gluconeogenesis in the Absence of Cystathionine Gamma-Lyase and the Underlying Mechanisms.Antioxidants & redox signaling · 2016Article
- Mini-review: diabetic renal complications, a potential stinky remedy.American journal of physiology. Renal physiology · 2016Review
- Cysteine and hydrogen sulphide in the regulation of metabolism: insights from genetics and pharmacology.The Journal of pathology · 2016Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Reduced β-cell mass and increased activities of ATP-sensitive K(+) channels in pancreatic β cells are associated with the pathogenesis of diabetes. Cystathionine γ-lyase (CSE) is a major hydrogen sulfide (H(2)S)-producing enzyme in pancreatic β cells. Herein, we examine the effects of genetic and pharmacologic ablation of CSE on β-cell functions and their correlation with streptozotocin (STZ)-induced diabetes. Compared with wild-type mice, CSE knockout (CSE KO) mice that received STZ injections exhibited a delayed onset of diabetic status. The application of dl-propargylglycine (PPG) to inhibit CSE activity protected wild-type mice from STZ-induced hyperglycemia and hypoinsulinemia. STZ significantly increased pancreatic H(2)S production in wild-type mice but not in CSE KO mice. STZ induced more apoptotic β-cell death in wild-type mice than in CSE KO mice. STZ exposure decreased the viability of cultured INS-1E cells, which was partly reversed by PPG co-treatment. STZ also significantly stimulated H(2)S production in cultured INS-1E cells. In addition, STZ stimulated ATP-sensitive K(+) currents in pancreatic β cells from wild-type mice but not in the presence of PPG or in β cells from CSE KO mice. Sodium hydrosulfide injection instantly increased blood glucose, decreased plasma insulin, and deteriorated glucose tolerance in mice. Take together, these results provide evidence that the CSE/H(2)S system plays a critical role in regulating β-cell functions.
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Registered trials
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