| First Author | Fujita Y | Year | 2021 |
| Journal | Sci Rep | Volume | 11 |
| Issue | 1 | Pages | 982 |
| PubMed ID | 33441837 | Mgi Jnum | J:301617 |
| Mgi Id | MGI:6502278 | Doi | 10.1038/s41598-020-80209-0 |
| Citation | Fujita Y, et al. (2021) Angiotensin II type 1a receptor loss ameliorates chronic tubulointerstitial damage after renal ischemia reperfusion. Sci Rep 11(1):982 |
| abstractText | We investigate whether suppressing the activation of the angiotensin II type 1a receptor (AT1a) can ameliorate severe chronic tubulointerstitial damage (TID) after renal ischemia reperfusion (IR) using AT1a knockout homozygous (AT1a(-/-)) male mice. To induce severe chronic TID after renal IR, unilateral renal ischemia was performed via clamping of the right renal pedicle in both AT1a(-/-) and wild-type (AT1a(+/+)) mice for 45 min. While marked renal atrophy and severe TID at 70 days postischemia was induced in the AT1a(+/+) mice, such a development was not provoked in the AT1a(-/-) mice. Although the AT1a(+/+) mice were administered hydralazine to maintain the same systolic blood pressure (SBP) levels as the AT1a(-/-) mice with lower SBP levels, hydralazine did not reproduce the renoprotective effects observed in the AT1a(-/-) mice. Acute tubular injury at 3 days postischemia was similar between the AT1a(-/-) mice and the AT1a(+/+) mice. From our investigations using IR kidneys at 3, 14, and 28 days postischemia, the multiple molecular mechanisms may be related to prevention of severe chronic TID postischemia in the AT1a(-/-) mice. In conclusion, inactivation of the AT1 receptor may be useful in preventing the transition of acute kidney injury to chronic kidney disease. |
