H2S as a Physiologic Vasorelaxant: Hypertension in Mice with Deletion of Cystathionine γ-Lyase
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Summary
It is shown that H2S is physiologically generated by cystathionine γ-lyase (CSE) and that genetic deletion of this enzyme in mice markedly reduces H 2S levels in the serum, heart, aorta, and other tissues.
- Type
- article
- Published
- 2008-10-24
- Cited by
- 2,155
- References
- 30
- Access
- Open access
- OpenAlex
- https://openalex.org/W2054064167
- Semantic Scholar
- https://api.semanticscholar.org/CorpusID:9472601
Keywords
Cystathionine beta synthase, Cystathionine gamma-lyase, Nitric oxide, Hydrogen sulfide, Vasodilation
References
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- Carbon monoxide and hypertension
- Endothelial-dependent vasodilation is reduced in mesenteric arteries from superoxide dismutase knockout mice.
- Role of hydrogen sulphide in haemorrhagic shock in the rat: protective effect of inhibitors of hydrogen sulphide biosynthesis
- Two's company, three's a crowd: can H2S be the third endogenous gaseous transmitter?
- Sulfur reduction by human erythrocytes.
- Heme Oxygenase-2 Is Activated by Calcium-Calmodulin*
- Buthionine sulfoximine causes endothelium dependent hyper-relaxation and hypoadiponectinemia.
- Homocysteine and vascular disease
- Murine cystathionine gamma-lyase: complete cDNA and genomic sequences, promoter activity, tissue distribution and developmental expression.
- Hypertension in mice lacking the gene for endothelial nitric oxide synthase
- Elevated blood pressures in mice lacking endothelial nitric oxide synthase.
- Novel neural modulators.
- Inhibition of hydrogen sulfide generation contributes to gastric injury caused by anti-inflammatory nonsteroidal drugs.
- Cystathionine gamma-lyase overexpression inhibits cell proliferation via a H2S-dependent modulation of ERK1/2 phosphorylation and p21Cip/WAK-1.
Cited by
- Making and working with hydrogen sulfide: The chemistry and generation of hydrogen sulfide in vitro and its measurement in vivo: a review.
- MicroRNA‐21 represses human cystathionine gamma‐lyase expression by targeting at specificity protein‐1 in smooth muscle cells
- Transplant tolerance is associated with reduced expression of cystathionine-γ-lyase that controls IL-12 production by dendritic cells and TH-1 immune responses.
- Involvement of redox‐signalling in endogenous hydrogen sulfide production
- Beyond H2S and NO interplay: hydrogen sulfide and nitroprusside react directly to give nitroxyl (HNO). A new pharmacological source of HNO.
- Hydrogen sulfide as a vasculoprotective factor
- Oxygen Sensing by the Carotid Body: Is It All Just Rotten Eggs?
- Inhibition of NADPH oxidase 4-related signaling by sodium hydrosulfide attenuates myocardial fibrotic response.
- Primary hepatocytes from mice lacking cysteine dioxygenase show increased cysteine concentrations and higher rates of metabolism of cysteine to hydrogen sulfide and thiosulfate
- Decreased Cystathionine-γ-lyase (CSE) Activity in Livers of Type 1 Diabetic Rats and Peripheral Blood Mononuclear Cells (PBMC) of Type 1 Diabetic Patients*
- Exogenous hydrogen sulfide causes different hemodynamic effects in normotensive and hypertensive rats via neurogenic mechanisms
- Wnt/β-catenin signaling induces the transcription of cystathionine-γ-lyase, a stimulator of tumor in colon cancer.
- A High‐Sensitivity Coumarin‐Based Fluorescent Probe for Monitoring Hydrogen Sulfide in Living Cells
- Hydrogen sulfide interacts with calcium signaling to enhance the chromium tolerance in Setaria italica.
- H2S restores the cardioprotection from ischemic post‐conditioning in isolated aged rat hearts
- A hexaphenylbenzene based AIEE active two photon probe for the detection of hydrogen sulfide with tunable self-assembly in aqueous media and application in live cell imaging.
- Therapeutic application of hydrogen sulfide donors: the potential and challenges
- Role of Gasotransmitters in Oxidative Stresses, Neuroinflammation, and Neuronal Repair
- Chemical Speciation of Selenium and Mercury as Determinant of Their Neurotoxicity.
- Cystathionine γ-Lyase Is Involved in the Renoprotective Effect of Brief and Repeated Ischemic Postconditioning After Renal Ischemia/Reperfusion Injury in Diabetes Mellitus.
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