Format

Send to

Choose Destination
Chin Med J (Engl). 2017 Aug 20;130(16):1980-1986. doi: 10.4103/0366-6999.211895.

Homocysteine: A Potential Common Route for Cardiovascular Risk and DNA Methylation in Psoriasis.

Author information

1
Department of Dermatology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100730, China.

Abstract

OBJECTIVE:

Homocysteine is a sulfur-containing amino acid with potential clinical significance. Abnormal homocysteine levels have been found in patients with psoriasis. This review summarizes the possible correlations among homocysteine, cardiovascular risk, and DNA methylation in psoriasis.

DATA SOURCES:

We retrieved the articles published in English from the PubMed database up to January 2017, using the keywords including "psoriasis," "homocysteine," "cardiovascular risk," "DNA methylation," "methylenetetrahydrofolate reductase," "MTHFR," and "MTHFR C677T."

STUDY SELECTION:

Articles about the roles of homocysteine in the cardiovascular risk and DNA methylation in psoriasis were obtained and reviewed.

RESULTS:

Observational studies consistently reported that elevated homocysteine is an independent risk factor for cardiovascular diseases. Several studies also consistently reported an association between psoriasis and increased cardiovascular risk. A substantial body of evidence also suggested that an elevated homocysteine level is related to the demethylation of DNA. Data from clinical trials also demonstrated that MTHFR C677T polymorphisms as well as DNA methylation aberrations are associated with psoriasis.

CONCLUSIONS:

This review highlighted the relationships among homocysteine, cardiovascular risk, and DNA methylation, suggesting that homocysteine may be a biological link between cardiovascular risk and DNA methylation in psoriasis.

PMID:
28776552
PMCID:
PMC5555134
DOI:
10.4103/0366-6999.211895
[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Wolters Kluwer Icon for PubMed Central
Loading ...
Support Center