Here we compared younger men (22 ± 2 yr, n = 26), middle-aged men (31 ± 5 yr, n = 35), older men without CAD (60 ± 10 yr, n = 30) and older men with CAD (63 ± 8 yr, n = 30) in terms of testosterone/estradiol ratio, leukocyte telomerase reverse transcriptase (hTERT) expression, activity of telomerase in peripheral blood mononuclear cells (PBMCs), and length of PBMC telomeres.
The aim of the present study was to determine whether six variants in the TERT gene are associated with risk of incident coronary heart disease, incident ischemic stroke, and mortality in participants in the biracial population-based Atherosclerosis Risk in Communities (ARIC) study, including rs2736100 that was found to influence mean telomere length in a genome-wide analysis.
Familial hypercholesterolemia (FH) is caused by mutations in the LDL receptor (LDLR) gene and is usually associated with hypercholesterolemia, lipid deposition in tissues, and premature coronary artery disease (CAD).
Loss-of-function mutations in PCSK9 result in significantly decreased LDL-cholesterol levels and a disproportionately large reduction in coronary heart disease risk by reducing the exposure to LDL-cholesterol throughout life.
Together, these data suggest that miR-224 interaction with the TCF21 transcript contributes to allelic imbalance of this gene, thus partly explaining the genetic risk for coronary heart disease associated at 6q23.2.
Patients with two abnormal LDL receptor genes (homozygous deficient patients) have severe hypercholesterolemia and life-threatening coronary artery disease in childhood.
These results indicate that the E670G polymorphism of the PCSK9 gene modulates plasma LDL-C levels, but that it is not a risk variant for CAD in ethnic Chinese in Taiwan.
Background Plasma proprotein convertase subtilisin/kexin type 9 (PCSK9) has been reported to be related to several risk factors and diseases such as inflammatory markers and coronary artery disease.
The aim of this study was to investigate the role of endothelial nitric oxide synthase (eNOS) gene intron 4 a/b variable number of tandem repeats (VNTR) polymorphism and other risk factors in the development of CAD in subjects living in Southern Turkey.
However, clinical impacts of lipoprotein(a) levels on adverse vascular events in patients with established coronary artery disease who are undergoing statin treatment have not been fully elucidated.
Pro-inflammatory interleukin-1 genotypes potentiate the risk of coronary artery disease and cardiovascular events mediated by oxidized phospholipids and lipoprotein(a).
Significantly reduced expression of all INK4/ARF transcripts (p15(INK4b), p16(INK4a), ARF and ANRIL) was found in PBTL of individuals harboring a common SNP (rs10757278) associated with increased risk of coronary artery disease, stroke and aortic aneurysm.
We review here the current understanding of PCSK9 and its potential as a therapeutic target through which to reduce LDL cholesterol for prevention and treatment of coronary heart disease.
Elevated levels of lipoprotein(a) [Lp(a)] and the presence of small isoforms of apolipoprotein(a) [apo(a)] have been associated with coronary artery disease (CAD) in whites but not in African Americans.
The T allele of the missense Glu(298)Aspendothelial nitric oxide synthase gene polymorphism is associated with coronary heart disease in younger individuals with high atherosclerotic risk profile.
Lipoprotein (a) (Lp(a)), a well-established risk factor for coronary artery diseases (CAD), would also be anticipated to be associated in a similar manner with risk of type 2 diabetes mellitus (T2DM) based on the common soil hypothesis of etiology of T2DM and CAD.