ArticleExperimental and therapeutic medicine2024
Vascular endothelial cells of Mongolian gerbils are resistant to cholesterol-induced mitochondrial dysfunction and oxidative damage.
Article in Experimental and therapeutic medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Beyond Taste: The Impact of Chocolate on Cardiovascular and Steatotic Liver Disease Risk Factors.Nutrients · 2026Review
- Metabolic-Associated Fatty Liver Disease: The Influence of Oxidative Stress, Inflammation, Mitochondrial Dysfunctions, and the Role of Polyphenols.Pharmaceuticals (Basel, Switzerland) · 2024Review
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7 authors.
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Abstract
Atherosclerosis is essentially the leading factor behind occurrences of cardiovascular diseases (CVDs)-associated incidents, while mitochondrial dysfunction is also the main cause of atherosclerosis. The present study conducted a comparative analysis of mitochondrial function-related indicators in cholesterol-induced vascular endothelial cells (VECs) from Mongolian gerbils, Sprague-Dawley (SD) rats and humans. It reported that the inhibitory effect of cholesterol treatment on the viability of Mongolian gerbil VECs was markedly lower than the other two types of VECs at the same concentration. Following cholesterol treatment, mitochondrial DNA copy numbers, reactive oxygen species level, calcium concentration and mitochondrial membrane potential of Mongolian gerbil VECs did not change markedly. These results suggested that the function of mitochondria in the VECs of Mongolian gerbil is normal. Additionally, cholesterol treatment also did not alter the levels of superoxide dismutase, glutathione peroxidase, ATP, NADH-CoQ reductase and cytochrome
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