The DOI matches its Crossref record; 3 of the 3 references it cites were found in a registry or an index.
Homocysteine metabolism, hyperhomocysteinaemia and vascular disease: An overview
Abstract
Summary: Hyperhomocysteinaemia has been regarded as a new modifiable risk factor for atherosclerosis and vascular disease. Homocysteine is a branch‐point intermediate of methionine metabolism, which can be further metabolised via two alternative pathways: degraded irreversibly through the transsulphuration pathway or remethylated to methionine by the remethylation pathway. Both pathways are B‐vitamin‐dependent. Plasma homocysteine concentrations are determined by nongenetic and genetic factors. The metabolism of homocysteine, the role of B vitamins and the contribution of nongenetic and genetic determinants of homocysteine concentrations are reviewed. The mechanisms whereby homocysteine causes endothelial damage and vascular disease are not fully understood. Recently, a link has been postulated between homocysteine, or its intermediates, and an alterated DNA methylation pattern. The involvement of epigenetic mechanisms in the context of homocysteine and atherosclerosis, due to inhibition of transmethylation reactions, is briefly overviewed.
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Citations
Cites
Okano, M., Bell, D. W., Haber, D. A., & Li, E. (1999) · Cell · doi:10.1016/s0092-8674(00)81656-6 · Cited by 6,143
Effects of DNA methylation on DNA-binding proteins and gene expression
Tate, P. H., & Bird, A. P. (1993) · Current Opinion in Genetics & Development · doi:10.1016/0959-437x(93)90027-m · Cited by 737 · cited 3×
“Moreover, methylation of GpG islands within the promoter regions inhibits the binding of transcription factors, thereby inhibiting gene transcription (Iguchi-Ariga and Schaffner 1989; Klangby et al 1998; Tate and Bird 1993).”
BackgroundIguchi-Ariga, S. M., & Schaffner, W. (1989) · Genes & Development · doi:10.1101/gad.3.5.612 · Cited by 559
Cited by
Neural tube defects and folate: case far from closed
Blom, H. J., Shaw, G. M., den Heijer, M., & Finnell, R. H. (2006) · Nature Reviews Neuroscience · doi:10.1038/nrn1986 · Cited by 562
Self-citationHomocysteine lowering interventions for preventing cardiovascular events
Martí-Carvajal, A. J., Solà, I., Lathyris, D., & Salanti, G. (2009) · Cochrane Database of Systematic Reviews · doi:10.1002/14651858.cd006612.pub2 · Cited by 520
The Contribution of Homocysteine Metabolism Disruption to Endothelial Dysfunction: State-of-the-Art
Esse, R., Barroso, M., Tavares de Almeida, I., & Castro, R. (2019) · International Journal of Molecular Sciences · doi:10.3390/ijms20040867 · Cited by 336
Self-citationHomocysteine-lowering interventions for preventing cardiovascular events
Martí-Carvajal, A. J., Solà, I., & Lathyris, D. (2015) · Cochrane Database of Systematic Reviews · doi:10.1002/14651858.cd006612.pub4 · Cited by 113
Rai, V. (2017) · Molecular Neurobiology · doi:10.1007/s12035-016-9722-8 · Cited by 88
Metadata
- Authors
- Castro, R., Rivera, I., Blom, H. J., Jakobs, C., & de Almeida, I. T.
- Venue
- Journal of Inherited Metabolic Disease
- Publisher
- Wiley
- Published
- 2006-02
- Volume
- 29
- Issue
- 1
- Pages
- 3-20
- ISSN
- 0141-8955 (ISSN-L)
- 1573-2665
- OpenAlex
- W2054476774
- Cited by
- 312
- References
- 3
- FWCI
- 11.36
- Type
- journal article
- Language
- en
- Open access
- closed
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- Castro, R., Rivera, I., Blom, H. J., Jakobs, C., & de Almeida, I. T. (2006). Homocysteine metabolism, hyperhomocysteinaemia and vascular disease: An overview. Journal of Inherited Metabolic Disease. https://doi.org/10.1007/s10545-006-0106-5
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