ReviewCurrent rheumatology reports2009
Atherosclerosis in autoimmune diseases.
Review in Current rheumatology reports, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 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
12 citing papers in PubMed, 33 citations in OpenAlex.
- The association among antioxidant enzymes, autoantibodies, and disease severity score in systemic lupus erythematosus: comparison of neuropsychiatric and nonneuropsychiatric groups.BioMed research international · 2014Trial
- Autoimmune thyroiditis and celiac disease do not worsen endothelial function in subjects with type 1 diabetes: an observational study.Diabetology & metabolic syndrome · 2022Article
- Association of serum levels of antibodies against ALDOA and FH4 with transient ischemic attack and cerebral infarction.BMC neurology · 2021Article
- Therapeutic Potential and Immunomodulatory Role of Coenzyme QAntioxidants (Basel, Switzerland) · 2021Review
- Case Report: A Case of Unusual Combination of Hypothyroidism, Myocardial Bridging, and Myocardial Infarction-Induced Left Ventricular Aneurysm.Frontiers in cardiovascular medicine · 2021Article
- Analysis of Drug Effects on Primary Human Coronary Artery Endothelial Cells Activated by Serum Amyloid A.Mediators of inflammation · 2018Article
- LDLR and PCSK9 Are Associated with the Presence of Antiphospholipid Antibodies and the Development of Thrombosis in aPLA Carriers.PloS one · 2016Article
- Simvastatin Efficiently Lowers Small LDL-IgG Immune Complex Levels: A Therapeutic Quality beyond the Lipid-Lowering Effect.PloS one · 2016Article
- The multiple faces of RAGE--opportunities for therapeutic intervention in aging and chronic disease.Expert opinion on therapeutic targets · 2016Review
- Dendritic cells, antibodies reactive with oxLDL, and inflammation.Journal of dental research · 2012Review
- Hyperlipidaemia in paediatric patients: the role of lipid-lowering therapy in clinical practice.Drug safety · 2010Review
- Natural killer T cells and atherosclerosis: form and function meet pathogenesis.Journal of innate immunity · 2010Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lipid peroxidation occurs frequently in patients with systemic autoimmune diseases and contributes to autoimmune vascular inflammation. Oxidized low-density lipoprotein (oxLDL) interacts with beta2-glycoprotein I (beta2GPI), forming oxLDL/beta2GPI complexes. Circulating oxLDL/beta2GPI complexes and autoantibodies to these complexes have been demonstrated in patients with systemic lupus erythematosus and antiphospholipid syndrome. These findings suggest an immunogenic nature of the complexes and an active proatherogenic role in autoimmunity. Biochemical characterization of the complexes and immunohistochemical studies of atherosclerotic lesions suggest that most of the complexes originate in the arterial wall and are released into circulation. The in vitro macrophage uptake of oxLDL/beta2GPI complexes increased significantly in the presence of antiphospholipid antibodies (anti-beta2GPI), suggesting that macrophage Fcgamma receptors are involved in the lipid intracellular influx that leads to foam cell formation. These findings provide an immunologic explanation for the accelerated development of atherosclerosis seen in systemic lupus erythematosus and antiphospholipid syndrome.
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.