2023
DOI: 10.3390/ijms24076783
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Atorvastatin Can Modulate DNA Damage Repair in Endothelial Cells Exposed to Mitomycin C

Abstract: HMG-CoA reductase inhibitors (statins) are widely used in the therapy of atherosclerosis and have a number of pleiotropic effects, including DNA repair regulation. We studied the cytogenetic damage and the expression of DNA repair genes (DDB1, ERCC4, and ERCC5) in human coronary artery (HCAEC) and internal thoracic artery endothelial cells (HITAEC) in vitro exposed to mitomycin C (MMC) (positive control), MMC and atorvastatin (MMC+Atv), MMC followed by atorvastatin treatment (MMC/Atv) and 0.9% NaCl (negative c… Show more

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Cited by 4 publications
(3 citation statements)
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“…This task requires large amounts of ATP to rearrange the intercellular junctions and maintain intracellular Ca 2+ metabolism, which is also indispensable for the enzymatic digestion and biosynthesis of nitric oxide and prostacyclin, the potent vasodilators [121][122][123][124]. With regards to nucleotide metabolism, DNA repair defects have been associated with age-related and premature endothelial dysfunction which develops as reduced nitric oxide release and chronic low-grade inflammation [125][126][127][128][129][130][131]. The same has been reported for decreased ubiquitination and impaired autophagy, as removal of dysfunctional organelles, supramolecular complexes, and molecules also becomes compromised with age [132][133][134], and ubiquitination participates in regulating rearrangements of intercellular junctions and integrity of the endothelial barrier [135,136].…”
Section: Discussionmentioning
confidence: 99%
“…This task requires large amounts of ATP to rearrange the intercellular junctions and maintain intracellular Ca 2+ metabolism, which is also indispensable for the enzymatic digestion and biosynthesis of nitric oxide and prostacyclin, the potent vasodilators [121][122][123][124]. With regards to nucleotide metabolism, DNA repair defects have been associated with age-related and premature endothelial dysfunction which develops as reduced nitric oxide release and chronic low-grade inflammation [125][126][127][128][129][130][131]. The same has been reported for decreased ubiquitination and impaired autophagy, as removal of dysfunctional organelles, supramolecular complexes, and molecules also becomes compromised with age [132][133][134], and ubiquitination participates in regulating rearrangements of intercellular junctions and integrity of the endothelial barrier [135,136].…”
Section: Discussionmentioning
confidence: 99%
“…Statins are widely used, but atropostatin(Atv) administration leads to oxidative stress and cellular damage. 213 Indicators of ferroptosis, such as iron overload, ROS accumulation, and lipid peroxidation, were observed in Atvtreated muscle cells, especially in the mitochondria of the cells. 214 One study reported that simvastatin causes ferroptosis in cancer cells by inhibiting HMGCR expression.…”
Section: Othersmentioning
confidence: 98%
“…(Veerabhadrappa et al, 2021). Atorvastatin can modulate the DNA damage repair response in primary human endothelial cells exposed to MMC in a cell line-and incubation scheme-dependent manner (Sinitsky et al, 2023).…”
Section: Dna Fragmentation Percentmentioning
confidence: 99%