2009
DOI: 10.1016/j.cca.2009.04.015
|View full text |Cite
|
Sign up to set email alerts
|

Genetic and environmental influences on total plasma homocysteine and coronary artery disease (CAD) risk among South Indians

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
4
1

Citation Types

2
20
1
2

Year Published

2011
2011
2019
2019

Publication Types

Select...
8
1

Relationship

0
9

Authors

Journals

citations
Cited by 50 publications
(25 citation statements)
references
References 35 publications
2
20
1
2
Order By: Relevance
“…Recent genetic epidemiological observations revealed that many genetic variants may increase the risk of CAD, including, for example, polymorphisms in angiotensin-converting enzyme [17], apolipoprotein E [18], hepatic lipase [19], platelet glycoprotein IIb/IIIa [20] and transforming growth factor-b [21]. The risk of developing CAD is influenced by a number of factors, including [22][23][24]. Recently, growing evidence has shown that inflammation is a critical factor in all stages of the CAD process, including atherosclerosis, plaque destabilization, plaque rupture and post-ischemia damage to the myocardium [3,25].…”
Section: Discussionmentioning
confidence: 99%
“…Recent genetic epidemiological observations revealed that many genetic variants may increase the risk of CAD, including, for example, polymorphisms in angiotensin-converting enzyme [17], apolipoprotein E [18], hepatic lipase [19], platelet glycoprotein IIb/IIIa [20] and transforming growth factor-b [21]. The risk of developing CAD is influenced by a number of factors, including [22][23][24]. Recently, growing evidence has shown that inflammation is a critical factor in all stages of the CAD process, including atherosclerosis, plaque destabilization, plaque rupture and post-ischemia damage to the myocardium [3,25].…”
Section: Discussionmentioning
confidence: 99%
“…It has also been observed that mild elevation or even moderate plasma Hcy is correlated with atherosclerosis [11]. Elevated plasma levels of Hcy injures endothelial cells [12,13], which increases oxidative modification of low-density lipoprotein-cholesterol (LDL-c) [14]. …”
Section: Introductionmentioning
confidence: 99%
“…All the above events are likely to trigger the cascade of events leading to atherosclerosis and arterial thrombosis. Several SNPs were reported in genes regulating the one-carbon metabolic pathway such as glutamate carboxypeptidase II (GCPII C1561T), reduced folate carrier 1 (RFC G80A), serine hydroxyl methyl transferase 1 (cSHMT C1420T), thymidylate synthase (TYMS 5 0 -UTR) 28 bp tandem repeat, methylenetetrahydrofolatereductase (MTHFR C677T) and 5-methyltetrahydrofolate homocysteine S-methyl transferase (MTR A2756G) interfere with the uptake of folate, folate carrier, DNA synthesis, synthesis of methyltetrahydrofolate, remethylation of HCY and reductive methylation of cobalamin, whereas the presence of 2R allele of functional polymorphism in TYMS, i.e., 28 bp tandem repeat in 5 0 -UTR (transcription enhancer element) was found to affect transcription process compared to 3R allele and might modulate folate flux.Among the different polymorphisms of one-carbon metabolism, GCPII C1561T [15]; MTHFR C677T [16], and MTR A2756G are studied extensively in CAD cases [17]. MTHFR C677T was observed to be associated with independent risk for CAD in the subjects with low folate status [18].…”
Section: Introductionmentioning
confidence: 98%