ArticleBritish journal of pharmacology2014
C-reactive protein promotes atherosclerosis by increasing LDL transcytosis across endothelial cells.
Article in British journal of pharmacology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 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
45 citing papers in PubMed, 82 citations in OpenAlex.
- Dual residual risk of lipid and inflammation: a prospective analysis of RCII on hypertension incidence and cardiovascular prognosis in Chinese and UK populations.BMC cardiovascular disorders · 2026Article
- Fluoxetine disrupts cholesterol metabolism in endothelial cells via SREBP2 activation.Translational psychiatry · 2026Article
- Article
- KAP1 SUMOylates and stabilizes SR-A to facilitate glycated LDL transcytosis and accelerate atherosclerosis.Cellular & molecular biology letters · 2026Article
- CAVIN-2 positively correlates with diabetic PAD and promotes LDL transcytosis by inhibiting eNOS activation.Annals of medicine · 2025Article
- Lipid raft proteomics identify endothelial myosin-9 (MYH9) as a regulator of low-density lipoprotein transcytosis and atherosclerosis.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Comparison of inflammatory cells, C-reactive protein, and lipid profile in atherosclerotic cardiovascular disease patients and healthy controls in Northwest Ethiopia.Scientific reports · 2025Article
- Targeting Mitochondrial Dysfunction to Prevent Endothelial Dysfunction and Atherosclerosis in Diabetes: Focus on the Novel Uncoupler BAM15.International journal of molecular sciences · 2025Review
- Effect of exercise on postprandial lipaemia in children with sickle cell disease.Frontiers in sports and active living · 2025Article
- The Jiangtang Tongmai Prescription Inhibits Inflammation and Fibrosis of Lung Fibroblast Autophagy Induced by Hyperglycemia by Regulating CAV1 Expression.Endocrine, metabolic & immune disorders drug targets · 2024Article
- AGEs promote atherosclerosis by increasing LDL transcytosis across endothelial cells via RAGE/NF-κB/Caveolin-1 pathway.Molecular medicine (Cambridge, Mass.) · 2023Article
- Caveolin-1 and Atherosclerosis: Regulation of LDLs Fate in Endothelial Cells.International journal of molecular sciences · 2023Review
- Effect of dual residual risk of cholesterol and inflammation on all-cause mortality in patients with cardiovascular disease.Cardiovascular diabetology · 2023Article
- Oscillating Glucose Induces the Increase in Inflammatory Stress through Ninjurin-1 Up-Regulation and Stimulation of Transport Proteins in Human Endothelial Cells.Biomolecules · 2023Article
- Inhibition of Vascular Endothelial Cadherin Cleavage Prevents Elastic Fiber Alterations and Atherosclerosis Induced by Intermittent Hypoxia in the Mouse Aorta.International journal of molecular sciences · 2022Article
- High-sensitivity C-reactive protein and low-density lipoprotein cholesterol association with incident of cardiovascular events: Isfahan cohort study.BMC cardiovascular disorders · 2022Article
- Skin aging: Dermal adipocytes metabolically reprogram dermal fibroblasts.BioEssays : news and reviews in molecular, cellular and developmental biology · 2022Article
- Relevance of lipoproteins, membranes, and extracellular vesicles in understanding C-reactive protein biochemical structure and biological activities.Frontiers in cardiovascular medicine · 2022Review
- Atherogenesis, Transcytosis, and the Transmural Cholesterol Flux: A Critical Review.Oxidative medicine and cellular longevity · 2022Review
- The Glycocalyx and Pressure-Dependent Transcellular Albumin Transport.Cardiovascular engineering and technology · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
16 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
background and purposeThe retention of plasma low-density lipoprotein (LDL) particles in subendothelial space following transcytosis across the endothelium is the initial step of atherosclerosis. Whether or not C-reactive protein (CRP) can directly affect the transcytosis of LDL is not clear. Here we have examined the effect of CRP on transcytosis of LDL across endothelial cells and have explored the underlying mechanisms. EXPERIMENTAL APPROACH: Effects of CRP on transcytosis of FITC-labelled LDL were examined with human umbilical vein endothelial cells and venous rings in vitro and, in vivo, ApoE(-/-) mice. Laser scanning confocal microscopy, immunohistochemistry and Oil Red O staining were used to assay LDL. KEY
resultsCRP increased transcytosis of LDL. An NADPH oxidase inhibitor, diphenylene iodonium, and the reducing agent, dithiothreitol partly or completely blocked CRP-stimulated increase of LDL transcytosis. The PKC inhibitor, bisindolylmaleimide I and the Src kinase inhibitor, PP2, blocked the trafficking of the molecules responsible for transcytosis. Confocal imaging analysis revealed that CRP stimulated LDL uptake by endothelial cells and vessel walls. In ApoE(-/-) mice, CRP significantly promoted early changes of atherosclerosis, which were blocked by inhibitors of transcytosis. CONCLUSIONS AND IMPLICATIONS: CRP promoted atherosclerosis by directly increasing the transcytosis of LDL across endothelial cells and increasing LDL retention in vascular walls. These actions of CRP were associated with generation of reactive oxygen species, activation of PKC and Src, and translocation of caveolar or soluble forms of the N-ethylmaleimide-sensitive factor attachment protein.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.