| External factors: | Atorvastatin |
| Aging type: | Prevent |
| Aging characteristic: |
| Category: | Chemical compounds |
| Phenotype: | Atherosclerosis |
| Experiment: | SA-β-gal activity assay//Telomere length assay |
| Description: | We incubated VSMCs with low-concentration t-BHP, which we have previously shown accelerates telomere shortening in culture.Senescence-associated β-galactosidase activity and telomere shortening were accelerated by t-BHP, but attenuated by atorvastatin treatment. |
| Target gene: | NBS-1//HDM2 |
| R-EF-Target gene: | --//Upregulation |
| Official symbol(s): | NBN//HDM2 |
| Target gene experiment: | Comet assay//Western blot |
| Target gene description: | In contrast, HDFnbs1-/- cells showed defective DNA repair, with incomplete repair even at 7 hours, which was not affected by atorvastatin.The induction of NBS-1 by atorvastatin at 15 minutes suggests that NBS-1 regulation is determined by posttranslational mechanisms. In VSMCs, atorvastatin pretreatment for 48 hours induced robust Ser166Hdm2 phosphorylation, which normalized 30 minutes after DNA damage, with minimal changes in total Hdm2 expression. |
| Regulatory pathway: | -- |
| R-EF-Pathway: | -- |
| Pathway experiment: | -- |
| Pathway description: | -- |
Annotation: