| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 10106304 | Journal of Surgical Research | 2019 | 10 Pages |
Abstract
The elevation of SOD2 and p53 protein acetylation in the mitochondria of renal tubular epithelial cells is an important signaling event in the pathogenesis of I/R-induced AKI. Thus, deacetylase SIRT3 may be an upstream regulator of both SOD2 and p53, and the SIRT3 deactivation may aggravate AKI.
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Authors
Jie MM, Zhenhua PhD, Haihong MB, Fei MD, Xinji MM, Wanlong MD,