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The Link Between Hyperhomocysteinemia and Hypomethylation: Implications for Cardiovascular Disease

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The Link Between Hyperhomocysteinemia and Hypomethylation: Implications for Cardiovascular Disease. / Barroso, Madalena; Handy, Diane E; Castro, Rita.

in: Journal of Inborn Errors of Metabolism and Screening (JIEMS), Jahrgang 5, 05.04.2020.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Review › Forschung

Harvard

Barroso, M, Handy, DE & Castro, R 2020, 'The Link Between Hyperhomocysteinemia and Hypomethylation: Implications for Cardiovascular Disease', Journal of Inborn Errors of Metabolism and Screening (JIEMS), Jg. 5. https://doi.org/10.1177/2326409817698994

APA

Barroso, M., Handy, D. E., & Castro, R. (2020). The Link Between Hyperhomocysteinemia and Hypomethylation: Implications for Cardiovascular Disease. Journal of Inborn Errors of Metabolism and Screening (JIEMS), 5. https://doi.org/10.1177/2326409817698994

Vancouver

Barroso M, Handy DE, Castro R. The Link Between Hyperhomocysteinemia and Hypomethylation: Implications for Cardiovascular Disease. Journal of Inborn Errors of Metabolism and Screening (JIEMS). 2020 Apr 5;5. https://doi.org/10.1177/2326409817698994

Bibtex

@article{698e1356aa9945cb9bddb1dd1c15748a,
title = "The Link Between Hyperhomocysteinemia and Hypomethylation: Implications for Cardiovascular Disease",
abstract = "ncreased levels of homocysteine have been established as a risk factor for cardiovascular disease (CVD) by mechanisms still incompletely defined. S-Adenosylhomocysteine (SAH) is the metabolic precursor of homocysteine that accumulates in the setting of hyperhomocysteinemia and is a negative regulator of most cell methyltransferases. Several observations, summarized in the current review, support the concept that SAH, rather than homocysteine, may be the culprit in the CVD risk that has been associated with hyperhomocysteinemia. This review examines the biosynthesis and catabolism of homocysteine and how these pathways regulate accumulation of SAH. In addition, the epidemiological and experimental links between hyperhomocysteinemia and CVD are discussed, along with the evidence suggesting a role for SAH in the disease. Finally, the effects of SAH on the hypomethylation of DNA, RNA, and protein are examined, with an emphasis on how specific molecular targets may be mediators of homocysteine-associated vascular disease.",
author = "Madalena Barroso and Handy, {Diane E} and Rita Castro",
year = "2020",
month = apr,
day = "5",
doi = "10.1177/2326409817698994",
language = "English",
volume = "5",
journal = "J Inborn Err Metab Scr (JIEMS)",
issn = "2326-4098",
publisher = "SAGE Publications",

}

RIS

TY - JOUR

T1 - The Link Between Hyperhomocysteinemia and Hypomethylation: Implications for Cardiovascular Disease

AU - Barroso, Madalena

AU - Handy, Diane E

AU - Castro, Rita

PY - 2020/4/5

Y1 - 2020/4/5

N2 - ncreased levels of homocysteine have been established as a risk factor for cardiovascular disease (CVD) by mechanisms still incompletely defined. S-Adenosylhomocysteine (SAH) is the metabolic precursor of homocysteine that accumulates in the setting of hyperhomocysteinemia and is a negative regulator of most cell methyltransferases. Several observations, summarized in the current review, support the concept that SAH, rather than homocysteine, may be the culprit in the CVD risk that has been associated with hyperhomocysteinemia. This review examines the biosynthesis and catabolism of homocysteine and how these pathways regulate accumulation of SAH. In addition, the epidemiological and experimental links between hyperhomocysteinemia and CVD are discussed, along with the evidence suggesting a role for SAH in the disease. Finally, the effects of SAH on the hypomethylation of DNA, RNA, and protein are examined, with an emphasis on how specific molecular targets may be mediators of homocysteine-associated vascular disease.

AB - ncreased levels of homocysteine have been established as a risk factor for cardiovascular disease (CVD) by mechanisms still incompletely defined. S-Adenosylhomocysteine (SAH) is the metabolic precursor of homocysteine that accumulates in the setting of hyperhomocysteinemia and is a negative regulator of most cell methyltransferases. Several observations, summarized in the current review, support the concept that SAH, rather than homocysteine, may be the culprit in the CVD risk that has been associated with hyperhomocysteinemia. This review examines the biosynthesis and catabolism of homocysteine and how these pathways regulate accumulation of SAH. In addition, the epidemiological and experimental links between hyperhomocysteinemia and CVD are discussed, along with the evidence suggesting a role for SAH in the disease. Finally, the effects of SAH on the hypomethylation of DNA, RNA, and protein are examined, with an emphasis on how specific molecular targets may be mediators of homocysteine-associated vascular disease.

U2 - 10.1177/2326409817698994

DO - 10.1177/2326409817698994

M3 - SCORING: Review article

VL - 5

JO - J Inborn Err Metab Scr (JIEMS)

JF - J Inborn Err Metab Scr (JIEMS)

SN - 2326-4098

ER -