In humans,<unk>  is directly involved in the development of atherosclerosis, which is the process responsible for the majority of cardiovascular diseases, due to accumulation of<unk> -cholesterol in the blood . Hyperthyroidism may be associated with hypocholesterolemia via upregulation of the<unk> , and hypothyroidism with the converse. A vast number of studies have described the relevance of<unk> s in the pathophysiology of atherosclerosis, metabolic syndrome, and steatohepatitis. Previously, rare mutations in<unk> -genes have been shown to contribute to myocardial infarction risk in individual families, whereas common variants at more than 45 loci have been associated with myocardial infarction risk in the population. When compared with non-carriers,<unk> R mutation carriers had higher plasma<unk>  cholesterol, whereas APOA5 mutation carriers had higher plasma triglycerides. Recent evidence has connected MI risk with coding-sequence mutations at two genes functionally related to APOA5, namely lipoprotein lipase and apolipoprotein C-III. Combined, these observations suggest that, as well as<unk>  cholesterol, disordered metabolism of triglyceride-rich lipoproteins contributes to MI risk. Overall,<unk> R has a high clinical relevance in blood lipids. Clinical marker A multi-locus genetic risk score study based on a combination of 27 loci, including the<unk> R gene, identified individuals at increased risk for both incident and recurrent coronary artery disease events, as well as an enhanced clinical benefit from statin therapy. The study was based on a community cohort study (the Malmö Diet and Cancer study) and four additional randomized controlled trials of primary prevention cohorts (JUPITER and ASCOT) and secondary prevention cohorts (CARE and PROVE IT-TIMI 22).
LDL receptor
Low-density lipoprotein receptor gene family
Heart-type fatty acid binding protein
Apolipoprotein
Lipoprotein lipase
Tumor-associated glycoprotein 72
Platelet membrane glycoprotein
Cystic fibrosis transmembrane conductance regulator