Because oxidative stress is one of the main causes of

Because oxidative stress is one of the main causes of senescence, we further investigated whether antioxidant therapy can protect renal tubal cells from premature cisplatin-induced senescence and slow down the progression of MCC after ARF. The activation of SIRT1 and the deactivation of p53 could be identified as potential targets to prevent premature renal aging and slow down the progression of MCC after ARF. These results suggest that cisplatin may lead to premature renal aging, which is associated with the development of cisplatin-induced CRI after ARF. The aim of this study was to determine whether cisplatinum induces premature renal aging and the role of premature renal aging in the progression of CKL according to ARF. N-acetylcysteine improves cisplatin-induced renal aging and interstitial renal fibrosis by activating sirtuin1 and p53 diacetillation. In a rat model with multiple cisplatin treatment, interstitial renal fibrosis was associated with premature renal aging. Poorly repaired renal tubercle cells showed signs of premature senescence. N-acetylcysteine improves cisplatin-induced renal senescence and interstitial renal fibrosis. We found that cisplatin induces premature renal aging in vitro and in vivo. These premature senescent cells can produce pro-fibrotic factors that promote organ fibrosis. By providing the information herein, we are not diagnosing, treating, curing, alleviating or preventing any disease or condition. Before starting any natural, integrative or conventional treatment, it is advisable to seek the advice of a recognized health professional. Poorly adapted repair has been identified by AKI as an important mechanism of IQC.

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