Vasodilatation caused by endogenous hydrogen sulfide in chronic renal failure
| Autor: | Af, Perna, Lanza D, Sepe I, Di Nunzio A, Conzo G, Satta E, Giovambattista Capasso, Ingrosso D |
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| Přispěvatelé: | Perna, A, Lanza, D, Sepe, I, Di Nunzio, A, Conzo, G, Satta, E, Capasso, G, Ingrosso, D |
| Jazyk: | italština |
| Rok vydání: | 2013 |
| Předmět: |
Inflammation
Mice Knockout Lyases Apoptosis Blood Pressure Kidney equipment and supplies Rats Vasodilation Mice Oxidative Stress Cardiovascular Diseases Enzyme Induction Disease Progression Animals Humans Kidney Failure Chronic Cysteine Hydrogen Sulfide Lipid Peroxidation Apoptosis Regulatory Proteins Homocysteine Cells Cultured |
| Zdroj: | Europe PubMed Central |
| Popis: | Hydrogen sulfide, (H2S), is an endogenous gas which exerts a protective function in several biological processes, including those involved in inflammation, blood pressure regulation, and energy metabolism. The enzymes involved in H2S production are cysthationine -synthetase, cysthationine -lyase and 3-mercaptopyruvate sulfurtransferase. Low plasma H2S levels have been found in chronic renal failure (CRF) in both humans and animal models. The mechanisms leading to H2S deficiency in CRF are linked to reduced gene expression of cysthationine -lyase. Intense research is currently under way to discover the link between low H2S levels, CRF progression and the uremic syndrome and to determine whether therapeutic interventions aimed at increasing H2S levels might benefit these patients. |
| Databáze: | OpenAIRE |
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