Homocysteine, hydrogen sulfide (H2S) and NMDA-receptor in heart failure

Neetu Tyagi, Paras K. Mishra, Suresh C. Tyagi

Research output: Contribution to journalReview article

11 Scopus citations

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 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.

Original languageEnglish (US)
Pages (from-to)441-446
Number of pages6
JournalIndian journal of biochemistry & biophysics
Volume46
Issue number6
StatePublished - Dec 1 2009

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry

Fingerprint Dive into the research topics of 'Homocysteine, hydrogen sulfide (H2S) and NMDA-receptor in heart failure'. Together they form a unique fingerprint.

  • Cite this