ArticleMediators of inflammation2014
Myeloperoxidase oxidized LDL interferes with endothelial cell motility through miR-22 and heme oxygenase 1 induction: possible involvement in reendothelialization of vascular injuries.
Article in Mediators of inflammation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 20 citations in OpenAlex.
- AGE induced macrophage-derived exosomes induce endothelial dysfunction in diabetes via miR-22-5p/FOXP1.Cardiovascular diabetology · 2025Article
- Bridging the gap between CVD and COVID-19: the oxidized LDL hypothesis.Frontiers in medicine · 2025Article
- A Potential Link between Myeloperoxidase Modified LDL, Atherosclerosis and Depression.International journal of molecular sciences · 2024Review
- TheInnate immunity · 2024Article
- Novel Insights into the Link Between Myeloperoxidase Modified LDL, LOX-1, and Neuroserpin in Stroke.Reviews in cardiovascular medicine · 2023Article
- Role of myeloperoxidase in inflammation and atherosclerosis (Review).Biomedical reports · 2022Review
- Unexpected Role of MPO-Oxidized LDLs in Atherosclerosis: In between Inflammation and Its Resolution.Antioxidants (Basel, Switzerland) · 2022Review
- Myeloperoxidase-Oxidized LDL Activates Human Aortic Endothelial Cells through the LOX-1 Scavenger Receptor.International journal of molecular sciences · 2022Article
- The effect of myeloperoxidase-oxidized LDL on THP-1 macrophage polarization and repolarization.Innate immunity · 2022Article
- Effect of myeloperoxidase modified LDL on bovine and human aortic endothelial cells.Experimental and therapeutic medicine · 2019Article
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cardiovascular disease linked to atherosclerosis is the leading cause of death worldwide. Atherosclerosis is mainly linked to dysfunction in vascular endothelial cells and subendothelial accumulation of oxidized forms of LDL. In the present study, we investigated the role of myeloperoxidase oxidized LDL (Mox-LDL) in endothelial cell dysfunction. We studied the effect of proinflammatory Mox-LDL treatment on endothelial cell motility, a parameter essential for normal vascular processes such as angiogenesis and blood vessel repair. This is particularly important in the context of an atheroma plaque, where vascular wall integrity is affected and interference with its repair could contribute to progression of the disease. We investigated in vitro the effect of Mox-LDL on endothelial cells angiogenic properties and we also studied the signalling pathways that could be affected by analysing Mox-LDL effect on the expression of angiogenesis-related genes. We report that Mox-LDL inhibits endothelial cell motility and tubulogenesis through an increase in miR-22 and heme oxygenase 1 expression. Our in vitro data indicate that Mox-LDL interferes with parameters associated with angiogenesis. They suggest that high LDL levels in patients would impair their endothelial cell capacity to cope with a damaged endothelium contributing negatively to the progression of the atheroma plaque.
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