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Published on: July 10, 2018

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

Neetu Tyagi1, Paras K Mishra, Suresh C Tyagi

  • 1Department of Physiology & Biophysics, School of Medicine University of Louisville Louisville, KY 40202, USA.

Indian Journal of Biochemistry & Biophysics
|April 6, 2010
PubMed

Insights

Hyperhomocysteinemia (HHcy) increases mitochondrial oxidative stress, but homocysteine (Hcy) can be converted to protective hydrogen sulfide (H2S). Gene therapy increasing cystathionine beta-synthase (CBS) may mitigate HHcy

Area of Science:

  • Cardiovascular Science
  • Mitochondrial Biology
  • Biochemistry

Background:

  • Mitochondrial matrix metalloproteinase (MMP) activation and oxidative stress mechanisms remain unclear.
  • Hyperhomocysteinemia (HHcy) elevates mitochondrial oxidative stress, contributing to cardiovascular remodeling and heart failure.
  • Homocysteine (Hcy) can be converted to hydrogen sulfide (H2S), a potent antioxidant, by cystathionine beta-synthase (CBS) and cystathionine gamma-lyase (CGL).

Purpose of the Study:

  • To elucidate the role of mitochondria in HHcy-induced cardiovascular damage.
  • To investigate the potential cardioprotective effects of H2S generated from Hcy.
  • To explore the therapeutic implications of enhancing Hcy to H2S conversion in vascular tissues.

Main Methods:

  • Mitochondrial localization and activation of MMPs by peroxynitrite.
  • Assessment of oxidative stress markers in mitochondria under HHcy conditions.
  • Analysis of Hcy metabolism to H2S via CBS and CGL enzyme activity.

Main Results:

  • MMPs are localized to mitochondria and activated by peroxynitrite, causing cardiovascular damage.
  • Elevated Hcy levels increase mitochondrial oxidative stress.
  • Hcy can be converted to cardioprotective H2S, but CBS is not ubiquitously present in vascular tissues.

Conclusions:

  • HHcy-induced mitochondrial oxidative stress contributes to cardiovascular dysfunction.
  • Hcy's paradoxical cardioprotective role is mediated by H2S production.
  • Gene therapy strategies to enhance CBS and CGL activity in vascular tissues hold potential for mitigating HHcy detrimental effects.

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