PMID- 20361707
OWN - NLM
STAT- MEDLINE
DCOM- 20101007
LR  - 20131121
IS  - 0301-1208 (Print)
IS  - 0301-1208 (Linking)
VI  - 46
IP  - 6
DP  - 2009 Dec
TI  - Homocysteine, hydrogen sulfide (H2S) and NMDA-receptor in heart failure.
PG  - 441-6
AB  - 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 beta-synthase (CBS) and cystathionine gamma-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.
FAU - Tyagi, Neetu
AU  - Tyagi N
AD  - Department of Physiology & Biophysics, School of Medicine University of 
      Louisville Louisville, KY 40202, USA.
FAU - Mishra, Paras K
AU  - Mishra PK
FAU - Tyagi, Suresh C
AU  - Tyagi SC
LA  - eng
PT  - Journal Article
PT  - Review
PL  - India
TA  - Indian J Biochem Biophys
JT  - Indian journal of biochemistry & biophysics
JID - 0310774
RN  - 0 (Receptors, N-Methyl-D-Aspartate)
RN  - 0LVT1QZ0BA (Homocysteine)
RN  - YY9FVM7NSN (Hydrogen Sulfide)
SB  - IM
MH  - Animals
MH  - Gene Deletion
MH  - Heart Failure/genetics/*metabolism/physiopathology
MH  - Homocysteine/*metabolism
MH  - Humans
MH  - Hydrogen Sulfide/*metabolism
MH  - Myocardial Contraction
MH  - Receptors, N-Methyl-D-Aspartate/deficiency/genetics/*metabolism
RF  - 31
EDAT- 2010/04/07 06:00
MHDA- 2010/10/12 06:00
CRDT- 2010/04/06 06:00
PHST- 2010/04/06 06:00 [entrez]
PHST- 2010/04/07 06:00 [pubmed]
PHST- 2010/10/12 06:00 [medline]
PST - ppublish
SO  - Indian J Biochem Biophys. 2009 Dec;46(6):441-6.