ArticleJournal of proteomics2011
Impact of HDL oxidation by the myeloperoxidase system on sterol efflux by the ABCA1 pathway.
Article in Journal of proteomics, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.
What it found
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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
18 citing papers in PubMed, 1 synthesis or guideline pooled it, 37 citations in OpenAlex.
- Association of rs2230806 in ABCA1 with coronary artery disease: An updated meta-analysis based on 43 research studies.Medicine · 2020Pooled it
- Nitrotyrosine, Nitrated Lipoproteins, and Cardiovascular Dysfunction in Patients with Type 2 Diabetes: What Do We Know and What Remains to Be Explained?Antioxidants (Basel, Switzerland) · 2022Review
- Post-Stroke Administration of L-4F Promotes Neurovascular and White Matter Remodeling in Type-2 Diabetic Stroke Mice.Frontiers in neurology · 2022Article
- High-Density Lipoproteins in Kidney Disease.International journal of molecular sciences · 2021Review
- Kidney as modulator and target of "good/bad" HDL.Pediatric nephrology (Berlin, Germany) · 2019Review
- Trends of Lipophilic, Antioxidant and Hematological Parameters Associated with Conventional and Electronic Smoking Habits in Middle-Age Romanians.Journal of clinical medicine · 2019Article
- Insights into the molecular mechanisms of diabetes-induced endothelial dysfunction: focus on oxidative stress and endothelial progenitor cells.Endocrine · 2015Article
- HDL-apolipoprotein A-I exchange is independently associated with cholesterol efflux capacity.Journal of lipid research · 2015Article
- Residual Cardiovascular Risk in Chronic Kidney Disease: Role of High-density Lipoprotein.Archives of medical research · 2015Review
- Article
- Redox-sensitive residue in the actin-binding interface of myosin.Biochemical and biophysical research communications · 2014Article
- High density lipoprotein is targeted for oxidation by myeloperoxidase in rheumatoid arthritis.Annals of the rheumatic diseases · 2013Article
- Recent advances in cardiovascular proteomics.Journal of proteomics · 2013Review
- Tyrosine modifications in aging.Antioxidants & redox signaling · 2012Review
- Crosstalk between reverse cholesterol transport and innate immunity.Trends in endocrinology and metabolism: TEM · 2012Review
- In Vivo Inflammation Does Not Impair ABCA1-Mediated Cholesterol Efflux Capacity of HDL.Cholesterol · 2012Article
- Anti-inflammatory and antioxidant properties of HDLs are impaired in type 2 diabetes.Diabetes · 2011Article
- Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Protein oxidation by phagocytic white blood cells is implicated in tissue injury during inflammation. One important target might be high-density lipoprotein (HDL), which protects against atherosclerosis by removing excess cholesterol from artery wall macrophages. In the human artery wall, cholesterol-laden macrophages are a rich source of myeloperoxidase (MPO), which uses hydrogen peroxide for oxidative reactions in the extracellular milieu. Levels of two characteristic products of MPO-chlorotyrosine and nitrotyrosine-are markedly elevated in HDL from human atherosclerotic lesions. Here, we describe how MPO-dependent chlorination impairs the ability of apolipoprotein A-I (apoA-I), HDL's major protein, to transport cholesterol by the ATP-binding cassette transporter A1 (ABCA1) pathway. Faulty interactions between apoA-I and ABCA1 are involved. Tandem mass spectrometry and investigations of mutated forms of apoA-I demonstrate that tyrosine residues in apoA-I are chlorinated in a site-specific manner by chloramine intermediates on suitably juxtaposed lysine residues. Plasma HDL isolated from subjects with coronary artery disease (CAD) also contains higher levels of chlorinated and nitrated tyrosine residues than HDL from healthy subjects. Thus, the presence of chlorinated HDL might serve as a marker of CAD risk. Because HDL damaged by MPO in vitro becomes dysfunctional, inhibiting MPO in vivo might be cardioprotective.
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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.