Please use this identifier to cite or link to this item:
Title: Homocysteine, Hydrogen sulfide (H2S) and NMDA-Receptor in Heart Failure
Authors: Tyagi, Neetu
Mishra, Paras K
Tyagi, Suresh C
Keywords: Mitochondrial matrix metalloproteinase
Myocyte mechanics
Calcium transient
Mitochondrial permeability
Hydrogen sulfide
Cystathionine β-synthase Cystathionine -lyase
Issue Date: Dec-2009
Publisher: CSIR
Abstract: Mitochondrial mechanism of oxidative stress and matrix metalloproteinase (MMP) activation was unclear. Our recent data suggested that MMPs are localized to mitochondria and activated by peroxynitrite, which causes cardiovascular remodeling and failure. Recently, we have demonstrated that elevated levels of homocysteine (Hcy), known as hyperhomocysteinemia (HHcy) increase oxidative stress in the mitochondria. Although HHcy causes heart failure, interestingly, it is becoming very clear that Hcy can generate hydrogen sulfide (H2S), if the enzymes cystathionine β-synthase (CBS) and cystathionine -lyase (CGL) are present. H2S is a strong anti-oxidant and vasorelaxing agent. Paradoxically, it is interesting that Hcy, a precursor of H2S can be cardioprotective. The CGL is ubiquitous, while the CBS is not present in the vascular tissues. Therefore, under normal condition, only half of Hcy can be converted to H2S. However, there is strong potential for gene therapy of CBS to vascular tissue that can mitigate the detrimental effects of Hcy by converting it to H2S. This scenario is possible, if the activities of both the enzymes (CBS and CGL) are increased in tissues by gene therapy.
Description: 441-446
ISSN: 0975-0959 (Online); 0301-1208 (Print)
Appears in Collections:IJBB Vol.46(6) [December 2009]

Files in This Item:
File Description SizeFormat 
IJBB 46(6) 441-446.pdf92.39 kBAdobe PDFView/Open

Items in NOPR are protected by copyright, with all rights reserved, unless otherwise indicated.