{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,4]],"date-time":"2026-04-04T12:47:17Z","timestamp":1775306837261,"version":"3.50.1"},"reference-count":46,"publisher":"Canadian Science Publishing","issue":"10","license":[{"start":{"date-parts":[[2017,10,1]],"date-time":"2017-10-01T00:00:00Z","timestamp":1506816000000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/www.nrcresearchpress.com\/page\/about\/CorporateTextAndDataMining"}],"content-domain":{"domain":["cdnsciencepub.com"],"crossmark-restriction":false},"short-container-title":["Appl. Physiol. Nutr. Metab."],"published-print":{"date-parts":[[2017,10]]},"abstract":"<jats:p> Homocysteine and its modulating genes have strongly emerged as novel biomarkers for coronary artery disease (CAD). In the present study, we investigated whether polymorphisms in homocysteine pathway genes and the plasma levels of homocysteine, folate, and vitamin B<jats:sub>12<\/jats:sub>, independently or in combination, are associated with CAD risk. A total of 504 participants were recruited (cases, n = 254; controls, n = 250, respectively). Tetra primer allele refractory mutation system polymerase chain reaction (PCR) was used for resolving the genotypes of 5\u203210\u2032 methylenetetrahydrofolate reductase \u2018MTHFR\u2019 polymorphisms (rs1801133, rs1801131), 5\u2032 methyl tetrahydrofolate homocysteine methyltransferase \u2018MTR\u2019 polymorphism (rs1805087), paroxanse1 \u2018PON1\u2019 polymorphism (rs662), and cystathionine beta synthase \u2018CBS\u2019 polymorphism (rs5742905). Conventional PCR amplification was carried out for resolving angiotensin converting enzyme \u2018ACE\u2019 insertion\/deletion (I\/D) polymorphism (rs4646994). ANOVA analysis, adjusted for the covariates, revealed that rs1801133, rs1805087 polymorphisms and homocysteine levels were associated with CAD. Logistic regression analysis (adjusted) revealed similar findings. Logistic regression analysis after applying factorial design to the studied single nucleotide polymorphisms (SNPs) revealed that homocysteine levels and heterozygous and mutant alleles at rs1801133, rs1805087, along with mutant alleles at rs1801131, rs4646994, conferred higher risk for CAD. Our results provide insight into the multifactorial nature of coronary artery disease. We highlight that SNPs in folate pathway genes and homocysteine have role in disease causation and can be used in disease prediction strategies. <\/jats:p>","DOI":"10.1139\/apnm-2017-0030","type":"journal-article","created":{"date-parts":[[2017,5,17]],"date-time":"2017-05-17T21:33:39Z","timestamp":1495056819000},"page":"1009-1014","update-policy":"https:\/\/doi.org\/10.1139\/csp-crossmark-policy","source":"Crossref","is-referenced-by-count":13,"title":["The communal relation of <i>MTHFR<\/i>, <i>MTR<\/i>, <i>ACE<\/i> gene polymorphisms and hyperhomocysteinemia as conceivable risk of coronary artery disease"],"prefix":"10.1139","volume":"42","author":[{"given":"Rizwan","family":"Masud","sequence":"first","affiliation":[{"name":"Division of Physiology, Department of Biomedical Sciences, College of Medicine, King Faisal University, Al Ahsa, 31982, Saudi Arabia."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Haider Zaigham","family":"Baqai","sequence":"additional","affiliation":[{"name":"Department of Medicine, Benazir Bhutto Hospital, Rawalpindi 46300, Pakistan."}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"155","reference":[{"key":"refg1\/ref1","doi-asserted-by":"publisher","DOI":"10.1016\/j.arcmed.2014.08.003"},{"key":"refg2\/ref2","doi-asserted-by":"publisher","DOI":"10.1177\/1076029616679505"},{"key":"refg3\/ref3","doi-asserted-by":"publisher","DOI":"10.1016\/j.thromres.2011.07.001"},{"key":"refg4\/ref4","doi-asserted-by":"publisher","DOI":"10.1253\/circj.CJ-12-0039"},{"key":"refg5\/ref5","doi-asserted-by":"publisher","DOI":"10.1016\/j.ancard.2008.05.018"},{"key":"refg6\/ref6","doi-asserted-by":"publisher","DOI":"10.1590\/S0104-42302009000300018"},{"key":"refg7\/ref7","doi-asserted-by":"publisher","DOI":"10.1139\/h04-050"},{"key":"refg8\/ref8","doi-asserted-by":"publisher","DOI":"10.1155\/2016\/2150763"},{"key":"refg9\/ref9","doi-asserted-by":"publisher","DOI":"10.1089\/dna.2011.1281"},{"key":"refg10\/ref10","doi-asserted-by":"publisher","DOI":"10.1016\/j.jvs.2016.01.056"},{"key":"refg11\/ref11","doi-asserted-by":"publisher","DOI":"10.1159\/000363008"},{"key":"refg12\/ref12","doi-asserted-by":"publisher","DOI":"10.1016\/j.transproceed.2006.10.224"},{"key":"refg13\/ref13","first-page":"545","volume":"29","author":"Du Y.","year":"2016","journal-title":"Biomed. 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