ArticleScientific reports2017
Influence of coronary artery disease and subclinical atherosclerosis related polymorphisms on the risk of atherosclerosis in rheumatoid arthritis.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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5 citing papers in PubMed, 18 citations in OpenAlex.
- Mutated CYP17A1 promotes atherosclerosis and early-onset coronary artery disease.Cell communication and signaling : CCS · 2023Article
- Identification of hub genes and transcription factors in patients with rheumatoid arthritis complicated with atherosclerosis.Scientific reports · 2022Article
- Article
- Genetics of Non-Alcoholic Fatty Liver and Cardiovascular Disease: Implications for Therapy?Frontiers in pharmacology · 2019Review
- Association of variant in the ADIPOQ gene and functional study for its role in atherosclerosis.Oncotarget · 2017Article
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Authors and funding
29 authors at 16 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A genetic component influences the development of atherosclerosis in the general population and also in rheumatoid arthritis (RA). However, genetic polymorphisms associated with atherosclerosis in the general population are not always involved in the development of cardiovascular disease (CVD) in RA. Accordingly, a study in North-American RA patients did not show the association reported in the general population of coronary artery disease with a series of relevant polymorphisms (TCF21, LPA, HHIPL1, RASD1-PEMT, MRPS6, CYP17A1-CNNM2-NT5C2, SMG6-SRR, PHACTR1, WDR12 and COL4A1-COL4A2). In the present study, we assessed the potential association of these polymorphisms with CVD in Southern European RA patients. We also assessed if polymorphisms implicated in the increased risk of subclinical atherosclerosis in non-rheumatic Caucasians (ZHX2, PINX1, SLC17A4, LRIG1 and LDLR) may influence the risk for CVD in RA. 2,609 Spanish patients were genotyped by TaqMan assays. Subclinical atherosclerosis was determined in 1,258 of them by carotid ultrasonography (assessment of carotid intima media thickness and presence/absence of carotid plaques). No statistically significant differences were found when each polymorphism was assessed according to the presence/absence of cardiovascular events and subclinical atherosclerosis, after adjustment for potential confounder factors. Our results do not show an association between these 15 polymorphisms and atherosclerosis in RA.
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