Homocysteine to hydrogen sulfide or hypertension

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

Research output: Contribution to journalReview articlepeer-review

133 Scopus citations


Hyperhomocysteinemia, an increased level of plasma homocysteine, is an independent risk factor for the development of premature arterial fibrosis with peripheral and cerebro-vascular, neurogenic and hypertensive heart disease, coronary occlusion and myocardial infarction, as well as venous thromboembolism. It is reported that hyperhomocysteinemia causes vascular dysfunction by two major routes: (1) increasing blood pressure and, (2) impairing the vasorelaxation activity of endothelial-derived nitric oxide. The homocysteine activates metalloproteinases and induces collagen synthesis and causes imbalances of elastin/collagen ratio which compromise vascular elastance. The metabolites from hyperhomocysteinemic endothelium could modify components of the underlying muscle cells, leading to vascular dysfunction and hypertension. Homocysteine metabolizes in the body to produce H2S, which is a strong antioxidant and vasorelaxation factor. At an elevated level, homocysteine inactivates proteins by homocysteinylation including its endogenous metabolizing enzyme, cystathionine γ-lyase. Thus, reduced production of H2S during hyperhomocysteinemia exemplifies hypertension and vascular diseases. In light of the present information, this review focuses on the mechanism of hyperhomocysteinemia-associated hypertension and highlights the novel modulatory role of H2S to ameliorate hypertension.

Original languageEnglish (US)
Pages (from-to)49-58
Number of pages10
JournalCell Biochemistry and Biophysics
Issue number2
StatePublished - 2010
Externally publishedYes


  • Homocysteine
  • Hydrogen sulfide
  • Hypertension
  • Vascular remodeling

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Cell Biology


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