Homocysteine to hydrogen sulfide or hypertension

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

Research output: Contribution to journalReview article

89 Citations (Scopus)

Abstract

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
Volume57
Issue number2
DOIs
StatePublished - Apr 13 2010
Externally publishedYes

Fingerprint

Hydrogen Sulfide
Hyperhomocysteinemia
Homocysteine
Blood Vessels
Hypertension
Vasodilation
Collagen
Cystathionine
Lyases
Elastin
Coronary Occlusion
Venous Thromboembolism
Blood pressure
Metalloproteases
Metabolites
Vascular Diseases
Muscle Cells
Endothelium
Muscle
Heart Diseases

Keywords

  • Homocysteine
  • Hydrogen sulfide
  • Hypertension
  • Vascular remodeling

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Cell Biology

Cite this

Homocysteine to hydrogen sulfide or hypertension. / Sen, Utpal; Mishra, Paras Kumar; Tyagi, Neetu; Tyagi, Suresh C.

In: Cell Biochemistry and Biophysics, Vol. 57, No. 2, 13.04.2010, p. 49-58.

Research output: Contribution to journalReview article

Sen, Utpal ; Mishra, Paras Kumar ; Tyagi, Neetu ; Tyagi, Suresh C. / Homocysteine to hydrogen sulfide or hypertension. In: Cell Biochemistry and Biophysics. 2010 ; Vol. 57, No. 2. pp. 49-58.
@article{b765f314b4eb442580d71185c7d62351,
title = "Homocysteine to hydrogen sulfide or hypertension",
abstract = "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.",
keywords = "Homocysteine, Hydrogen sulfide, Hypertension, Vascular remodeling",
author = "Utpal Sen and Mishra, {Paras Kumar} and Neetu Tyagi and Tyagi, {Suresh C.}",
year = "2010",
month = "4",
day = "13",
doi = "10.1007/s12013-010-9079-y",
language = "English (US)",
volume = "57",
pages = "49--58",
journal = "Cell Biochemistry and Biophysics",
issn = "1085-9195",
publisher = "Humana Press",
number = "2",

}

TY - JOUR

T1 - Homocysteine to hydrogen sulfide or hypertension

AU - Sen, Utpal

AU - Mishra, Paras Kumar

AU - Tyagi, Neetu

AU - Tyagi, Suresh C.

PY - 2010/4/13

Y1 - 2010/4/13

N2 - 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.

AB - 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.

KW - Homocysteine

KW - Hydrogen sulfide

KW - Hypertension

KW - Vascular remodeling

UR - http://www.scopus.com/inward/record.url?scp=77954142028&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=77954142028&partnerID=8YFLogxK

U2 - 10.1007/s12013-010-9079-y

DO - 10.1007/s12013-010-9079-y

M3 - Review article

VL - 57

SP - 49

EP - 58

JO - Cell Biochemistry and Biophysics

JF - Cell Biochemistry and Biophysics

SN - 1085-9195

IS - 2

ER -