ArticleJournal of vascular surgery2012
Hypercholesterolemia and oxidative stress inhibit endothelial cell healing after arterial injury.
Article in Journal of vascular surgery, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 43 citations in OpenAlex.
- iPLA2 inhibition blocks LysoPC-induced TRPC6 externalization and promotes Re-endothelialization of carotid injuries in hypercholesterolemic mice.Cell calcium · 2023Article
- Sprouty1 has a protective role in atherogenesis and modifies the migratory and inflammatory phenotype of vascular smooth muscle cells.Atherosclerosis · 2023Article
- p85α regulatory subunit isoform controls PI3-kinase and TRPC6 membrane translocation.Cell calcium · 2023Article
- Photobiomodulation reduces oxidative stress in diabetic wounded fibroblast cells by inhibiting the FOXO1 signaling pathway.Journal of cell communication and signaling · 2021Article
- Inhibition of P110α and P110δ catalytic subunits of PI3 kinase reverses impaired arterial healing after injury in hypercholesterolemic male mice.American journal of physiology. Cell physiology · 2021Article
- P110α and P110δ catalytic subunits of PI3 kinase regulate lysophosphatidylcholine-induced TRPC6 externalization.American journal of physiology. Cell physiology · 2021Article
- Notch pathway activation mediated the senescence of endothelial progenitor cells in hypercholesterolemic mice.Journal of bioenergetics and biomembranes · 2020Article
- Thymoquinone ameliorates Pachycondyla sennaarensis venom-induced acute toxic shock in male rats.BMC pharmacology & toxicology · 2019Article
- Effect of N-acetylcysteine on intimal hyperplasia and endothelial proliferation in rabbit carotid artery anastomosis.Archives of medical science : AMS · 2019Article
- Exosomes derived from M1 macrophages aggravate neointimal hyperplasia following carotid artery injuries in mice through miR-222/CDKN1B/CDKN1C pathway.Cell death & disease · 2019Article
- Delayed death following paraquat poisoning: three case reports and a literature review.Toxicology research · 2018Review
- The upregulated scavenger receptor CD36 is associated with the progression of nontarget lesions after stent implantation in atherosclerotic rabbits.Journal of inflammation research · 2018Article
- Integration of TRPC6 and NADPH oxidase activation in lysophosphatidylcholine-induced TRPC5 externalization.American journal of physiology. Cell physiology · 2017Article
- Delivery of Antioxidant and Anti-inflammatory Agents for Tissue Engineered Vascular Grafts.Frontiers in pharmacology · 2017Review
- Delayed reendothelialization with rapamycin is rescued by the addition of nicorandil in balloon-injured rat carotid arteries.Oncotarget · 2016Article
- Hypercholesterolemia inhibits re-endothelialization of arterial injuries by TRPC channel activation.Journal of vascular surgery · 2015Article
- Apolipoprotein A-I mimetic peptide reverses impaired arterial healing after injury by reducing oxidative stress.Atherosclerosis · 2015Article
- Phototherapy improves wound healing in rats subjected to high-fat diet.Lasers in medical science · 2015Article
- Limiting prolonged inflammation during proliferation and remodeling phases of wound healing in streptozotocin-induced diabetic rats supplemented with camel undenatured whey protein.BMC immunology · 2013Article
- Thrombin, a mediator of cerebrovascular inflammation in AD and hypoxia.Frontiers in aging neuroscience · 2013Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
objectiveEndothelial cell (EC) migration is essential for arterial healing after angioplasty. Oxidized low-density lipoproteins and oxidative stress decrease EC migration in vitro. The objective of this study was to determine the effect of hypercholesterolemia and oxidative stress on EC healing after an arterial injury.
methodsC57BL/6 wild-type mice were placed in one of eight groups: chow diet (n = 11), high-cholesterol (HC) diet (n = 11), chow diet plus paraquat (n = 11), HC diet plus paraquat (n = 11), chow diet plus N-acetylcysteine (NAC) (n = 11), HC diet plus NAC (n = 11), chow diet plus paraquat and NAC (n = 11), and HC diet plus paraquat and NAC (n = 11). After 2 weeks on the assigned diet with or without NAC, the carotid artery was injured using electrocautery. Animals in the paraquat groups were given 1 mg/kg intraperitoneally to increase oxidative stress. After 120 hours, Evans Blue dye was infused intravenously to stain the area of the artery that remained deendothelialized. This was used to calculate the percentage of re-endothelialization. Plasma and tissue samples were analyzed for measures of oxidative stress.
resultsThe HC diet increased oxidative stress and reduced EC healing compared with a chow diet, with EC covering 26.8% ± 2.8% and 48.1% ± 5.2% (P < .001) of the injured area, respectively. Administration of paraquat decreased healing in both chow and HC animals to 18.1% ± 3.5% (P < .001) and 9.8% ± 4.6% (P < .001), respectively. Pretreatment with NAC (120 mmol/L in drinking water) for 2 weeks prior to injury, to decrease oxidative stress, improved EC healing to 39.9% ± 5.7% (P < .001) in hypercholesterolemic mice and to 30.7% ± 3.6% (P < .001) in the paraquat group. NAC treatment improved healing to 24.6% ± 3.4% (P < .001) in hypercholesterolemic mice treated with paraquat.
conclusionRe-endothelialization of arterial injuries is reduced in hypercholesterolemic mice and is inversely correlated with oxidative stress. An oral antioxidant decreases oxidative stress and improves EC healing. CLINICAL RELEVANCE: Vascular injury following cardiovascular intervention, including cardiac and peripheral arterial angioplasty and stenting, is associated with inflammation and oxidative stress. Hypercholesterolemia is also associated with increased oxidative stress. Oxidative stress, regardless of the source, induces cellular dysfunction in endothelial and smooth muscle cells that reduce healing after arterial injury. Decreasing oxidative stress with an exogenously administered antioxidant can improve endothelial cell healing, and this is important to control intimal hyperplasia and reduce the thrombogenicity of the vessel.
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