| First Author | Zhou J | Year | 2020 |
| Journal | Am J Physiol Renal Physiol | Volume | 318 |
| Issue | 1 | Pages | F209-F215 |
| PubMed ID | 31813254 | Mgi Jnum | J:290480 |
| Mgi Id | MGI:6443710 | Doi | 10.1152/ajprenal.00516.2019 |
| Citation | Zhou J, et al. (2020) TAK1 deficiency attenuates cisplatin-induced acute kidney injury. Am J Physiol Renal Physiol 318(1):F209-F215 |
| abstractText | Cisplatin can cause acute kidney injury (AKI), but the molecular mechanisms are not well understood. The objective of the present study was to examine the role of transforming growth factor-beta-activated kinase-1 (TAK1) in the pathogenesis of cisplatin-induced AKI. Wild-type mice and proximal tubule TAK1-deficient mice were treated with vehicle or cisplatin. Compared with wild-type control mice, proximal tubule TAK1-deficient mice had less severe kidney dysfunction, tubular damage, and apoptosis after cisplatin-induced AKI. Furthermore, conditional disruption of TAK1 in proximal tubular epithelial cells reduced caspase-3 activation, proinflammatory molecule expression, and JNK phosphorylation in the kidney in cisplatin-induced AKI. Taken together, cisplatin activates TAK1-JNK signaling pathway to promote tubular epithelial cell apoptosis and inflammation in cisplatin-induced AKI. Targeting TAK1 could be a novel therapeutic strategy against cisplatin-induced AKI. |
