ReviewClinical cardiology1999
Pathophysiology of triglyceride-rich lipoproteins in atherothrombosis: cellular aspects.
Review in Clinical cardiology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
14 citing papers in PubMed, 70 citations in OpenAlex.
- Association between the cardiometabolic index and cardiovascular disease risk in patients with cardiovascular-kidney-metabolic syndrome: a cohort study.BMC cardiovascular disorders · 2025Article
- Triglyceride and Triglyceride-Rich Lipoproteins in Atherosclerosis.Frontiers in molecular biosciences · 2022Review
- Non-HDL as a Valid Surrogate Marker of Small Dense LDL in a Young Indian Population.Indian journal of clinical biochemistry : IJCB · 2019Article
- Elevated Levels of Very Low-density Lipoprotein Cholesterol Independently Associated with In-stent Restenosis in Diabetic Patients after Drug-eluting Stent Implantation.Chinese medical journal · 2017Article
- Very low density lipoprotein cholesterol associates with coronary artery calcification in type 2 diabetes beyond circulating levels of triglycerides.Atherosclerosis · 2014Article
- Lipoprotein subfractions and dietary intake of n-3 fatty acid: the Genetics of Coronary Artery Disease in Alaska Natives study.The American journal of clinical nutrition · 2012Article
- Lysosomes, cholesterol and atherosclerosis.Clinical lipidology · 2010Article
- Relation among lipoprotein subfractions and carotid atherosclerosis in Alaskan Eskimos (from the GOCADAN Study).The American journal of cardiology · 2009Article
- Transcriptional regulation of plasminogen activator inhibitor-1 in vascular endothelial cells induced by oxidized very low density lipoproteins.Molecular and cellular biochemistry · 2008Article
- Oxidation of chylomicron remnant-like particles inhibits their uptake by THP-1 macrophages by apolipoprotein E-dependent processes.Biochimica et biophysica acta · 2007Article
- Peroxisome proliferator-activated receptor delta promotes very low-density lipoprotein-derived fatty acid catabolism in the macrophage.Proceedings of the National Academy of Sciences of the United States of America · 2006Article
- Fenofibrate: a novel formulation (Triglide) in the treatment of lipid disorders: a review.International journal of nanomedicine · 2006Review
- Remnant lipoproteins and atherosclerosis.Current atherosclerosis reports · 2005Review
- Postprandial lipemia and cardiovascular disease.Current atherosclerosis reports · 2003Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Elevated plasma levels of triglyceride-rich lipoproteins (TGRLP), including very low-density lipoproteins (VLDL), chylomicrons, and their remnants, are now acknowledged as risk factors for cardiovascular disease. Interactions of TGRLP with lipoprotein receptors on monocytes, macrophages, and endothelial cells may be mechanistically linked to this risk. Triglyceride-rich lipoproteins from hypertriglyceridemic (HTG) subjects have the abnormal ability to bind to low-denisty lipoprotein receptors via apoE, and plasma chylomicrons from all subjects bind to a new, distinct receptor for apoB48 that is expressed specifically by monocytes, macrophages, and endothelial cells. Receptor binding and uptake of TGRLP by these cells are likely mechanisms involved in the formation of lipid-filled, macrophage-derived "foam cells" of atherosclerotic lesions and for defective fibrinolysis due to endothelial dysfunction. Recognition of the atherothrombogenic potential of TGRLP may lead to improved interventions to lessen or prevent the often fatal sequelae of coronary atherosclerosis and thrombosis associated with elevated plasma triglyceride levels.
Indexed as
Identifiers
What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.