ArticleAntioxidants & redox signaling2018
A Novel Mechanism for Atherosclerotic Calcification: Potential Resolution of the Oxidation Paradox.
Article in Antioxidants & redox signaling, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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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
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Who cites it
7 citing papers in PubMed, 8 citations in OpenAlex.
- Glycerol Monolaurate Supplementation in Extruded Diets Enhances Immune Function and Antioxidant Capacity and Alters the Gut Microbiota and Fecal Metabolome in Cats.Antioxidants (Basel, Switzerland) · 2026Article
- Negative Air Ions Attenuate Nicotine-Induced Vascular Endothelial Dysfunction by Suppressing AP1-Mediated FN1 and SPP1.Antioxidants (Basel, Switzerland) · 2025Article
- Association between the atherogenic index of plasma and abdominal aortic calcification: results from the National Health and Nutrition Examination Survey 2013-2014.Frontiers in endocrinology · 2025Article
- Inflammatory Cells in Atherosclerosis.Antioxidants (Basel, Switzerland) · 2022Review
- Induced pluripotent stem cell-derived smooth muscle cells to study cardiovascular calcification.Frontiers in cardiovascular medicine · 2022Article
- Non-alcoholic Fatty Liver Disease Is Associated With Aortic Calcification: A Cohort Study With Propensity Score Matching.Frontiers in endocrinology · 2022Article
- Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
aimIn this study, we tested the hypothesis that lipid peroxide-derived dicarboxylic acids (DCAs), by virtue of their ability to bind to calcium (Ca), might be involved in atherosclerotic calcification. We determined the ability of azelaic acid (AzA) to promote calcification in human aortic smooth muscle cells (HASMCs), identified AzA in human calcified atherosclerotic lesions, and compared its levels with control and noncalcified atherosclerotic lesions.
resultsHASMCs efficiently converted 9-oxononanoic acid (ONA), a lipid peroxide-derived monocarboxylic aldehyde, to AzA. In vitro incubations of AzA micelles with HASMC resulted in the formation of Ca deposits, which contained AzA. Liquid chromatography-mass spectrometry analysis of human control uninvolved artery, noncalcified, and calcified lesions showed significant increase of AzA in calcified lesions compared with noncalcified and control tissues. Calcified mouse atherosclerotic lesions also showed substantial presence of AzA in Ca complexes. INNOVATION: This study identifies a DCA, AzA, as an integral part of the Ca complex. The study also demonstrates the conversion of a lipid peroxidation product, ONA, as a potential source of AzA, and establishes the presence of AzA in calcified materials isolated from human and mouse lesions.
conclusionThe presence of AzA as a Ca sequestering agent in atherosclerotic lesions (i) might indicate participation of oxidized low-density lipoprotein (Ox-LDL) derived products in calcification, (ii) explain the potential correlation between calcification and overall plaque burden (as Ox-LDL has been suggested to be involved in atherogenesis), (iii) could contribute to plaque stabilization via its anti-inflammatory actions, and (iv) might explain why antioxidants failed to affect atherosclerosis in clinical studies. Antioxid. Redox Signal. 29, 471-483.
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Registered trials
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