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The central role of arterial retention of cholesterol-rich apolipoprotein-B-containing lipoproteins in the pathogenesis of atherosclerosis: a triumph of simplicity

Artikel i vetenskaplig tidskrift
Författare Jan Borén
Kevin Jon Williams
Publicerad i Current Opinion in Lipidology
Volym 27
Nummer/häfte 5
Sidor 473-483
ISSN 0957-9672
Publiceringsår 2016
Publicerad vid Institutionen för medicin, avdelningen för molekylär och klinisk medicin
Sidor 473-483
Språk en
Länkar dx.doi.org/10.1097/mol.000000000000...
Ämnesord apolipoprotein-B, atherosclerosis, Mendelian randomization studies, prospective randomized controlled trials, proteoglycan, low-density-lipoprotein, smooth-muscle-cells, proteoglycan-binding-site, e-deficient mice, atherogenic lipoproteins, promotes atherosclerosis, subendothelial retention, cardiovascular events, extracellular-matrix, metabolic syndrome, Biochemistry & Molecular Biology, Endocrinology & Metabolism, Cardiovascular System & Cardiology
Ämneskategorier Klinisk medicin

Sammanfattning

Purpose of reviewToday, it is no longer a hypothesis, but an established fact, that increased plasma concentrations of cholesterol-rich apolipoprotein-B (apoB)-containing lipoproteins are causatively linked to atherosclerotic cardiovascular disease (ASCVD) and that lowering plasma LDL concentrations reduces cardiovascular events in humans. Here, we review evidence behind this assertion, with an emphasis on recent studies supporting the response-to-retention' model - namely, that the key initiating event in atherogenesis is the retention, or trapping, of cholesterol-rich apoB-containing lipoproteins within the arterial wall.Recent findingsNew clinical trials have shown that ezetimibe and anti-PCSK9 antibodies - both nonstatins - lower ASCVD events, and they do so to the same extent as would be expected from comparable plasma LDL lowering by a statin. These studies demonstrate beyond any doubt the causal role of apoB-containing lipoproteins in atherogenesis. In addition, recent laboratory experimentation and human Mendelian randomization studies have revealed novel information about the critical role of apoB-containing lipoproteins in atherogenesis. New information has also emerged on mechanisms for the accumulation in plasma of harmful cholesterol-rich and triglyceride-rich apoB-containing remnant lipoproteins in states of overnutrition. Like LDL, these harmful cholesterol-rich and triglyceride-rich apoB-containing remnant lipoprotein remnants become retained and modified within the arterial wall, causing atherosclerosis.SummaryLDL and other cholesterol-rich, apoB-containing lipoproteins, once they become retained and modified within the arterial wall, cause atherosclerosis. This simple, robust pathophysiologic understanding may finally allow us to eradicate ASCVD, the leading killer in the world.

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