ArticleMolecular biology reports2012
N-acetyl cysteine suppresses the foam cell formation that is induced by oxidized low density lipoprotein via regulation of gene expression.
Article in Molecular biology reports, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05908513 (Randomized Study on N-acetylcysteine Treatment and Outcomes in Patients With Advanced Atherosclerotic Heart Diseases and Diabetes Mellitus), which is not on this map. Cited by 15 papers.
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.
Randomized Study on N-acetylcysteine Treatment and Outcomes in Patients With Advanced Atherosclerotic Heart Diseases and Diabetes Mellitus (RENEWAL)
Who cites it
15 citing papers in PubMed, 29 citations in OpenAlex.
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- Lipid-Laden Macrophages in Pulmonary Diseases.Cells · 2024Review
- Epigenetic mechanisms of alveolar macrophage activation in chemical-induced acute lung injury.Frontiers in immunology · 2024Review
- N-Acetylcysteine and Atherosclerosis: Promises and Challenges.Antioxidants (Basel, Switzerland) · 2023Review
- Beneficial in vitro effect of N-acetylcysteine and coenzyme Q10 on DNA damage in neurodegenerative Niemann-Pick type C 1 disease: preliminary results.Naunyn-Schmiedeberg's archives of pharmacology · 2023Article
- N‑acetyl cysteine prevents ambient fine particulate matter‑potentiated atherosclerosis via inhibition of reactive oxygen species‑induced oxidized low density lipoprotein elevation and decreased circulating endothelial progenitor cell.Molecular medicine reports · 2022Article
- Oxidized LDL-dependent pathway as new pathogenic trigger in arrhythmogenic cardiomyopathy.EMBO molecular medicine · 2021Article
- N‑acetylcysteine inhibits atherosclerosis by correcting glutathione‑dependent methylglyoxal elimination and dicarbonyl/oxidative stress in the aorta of diabetic mice.Molecular medicine reports · 2021Article
- Article
- Molecular mechanisms and genetic regulation in atherosclerosis.International journal of cardiology. Heart & vasculature · 2018Review
- Effect of N-Acetylcysteine on Dyslipidemia and Carbohydrate Metabolism in STZ-Induced Diabetic Rats.International journal of vascular medicine · 2018Article
- N-acetylcysteine inhibits in vivo oxidation of native low-density lipoprotein.Scientific reports · 2015Article
- Stearoyl-CoA Desaturase-1: Is It the Link between Sulfur Amino Acids and Lipid Metabolism?Biology · 2015Review
- Arachidonic acid-modified lovastatin discoidal reconstituted high density lipoprotein markedly decreases the drug leakage during the remodeling behaviors induced by lecithin cholesterol acyltransferase.Pharmaceutical research · 2014Article
- Low-density lipoprotein, its susceptibility to oxidation and the role of lipoprotein-associated phospholipase A2 and carboxyl ester lipase lipases in atherosclerotic plaque formation.Archives of medical science : AMS · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Foam cells derived from macrophages have been implicated as markers of early stage atherosclerosis development. In this study, we found that N-acetyl cysteine (NAC), a well-known inhibitor of reactive oxygen species (ROS), decreased the generation of ROS and suppressed foam cell formation in the presence of oxidized low density lipoprotein through down-regulation of cluster of differentiation 36 expression. We investigated gene expression profiles in order to determine the effects of NAC on foam cell formation using a microarray analysis. The level of apolipoprotein E, which is involved in lipid efflux, was increased and the levels of the antioxidant genes glutathione peroxidase 1 and 3 were also increased. The expression levels of the oxidative stress response and the DNA repair genes were decreased. These results were confirmed using quantitative real-time PCR. Our results indicate that oxidative stress plays an important role in foam cell formation, and that regulation of oxidation using antioxidants is a potential therapeutic method for blocking atherosclerosis development.
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Registered trials
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