Please use this identifier to cite or link to this item: http://nopr.niscair.res.in/handle/123456789/7247
Title: Homocysteine, Hydrogen sulfide (H<sub>2</sub>S) 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
NMDA-R1
Hydrogen sulfide
Cystathionine β-synthase Cystathionine <img src='/image/spc_char/gamma2.gif' border=0>-lyase
Homocysteine
Hyperhomocysteinemia
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 (H<sub>2</sub>S), if the enzymes cystathionine β-synthase (CBS) and cystathionine <img src='/image/spc_char/gamma2.gif' border=0>-lyase (CGL) are present. H<sub>2</sub>S is a strong anti-oxidant and vasorelaxing agent. Paradoxically, it is interesting that Hcy, a precursor of H<sub>2</sub>S 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 H<sub>2</sub>S. 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 H<sub>2</sub>S. This scenario is possible, if the activities of both the enzymes (CBS and CGL) are increased in tissues by gene therapy.
Description: 441-446
URI: http://hdl.handle.net/123456789/7247
ISSN: 0975-0959 (Online); 0301-1208 (Print)
Appears in Collections:IJBB Vol.46(6) [December 2009]

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