研究者情報

イチカワ　ダイスケ   ICHIKAWA DAISUKE   市川大介    所属   医学部医学科 腎臓・高血圧内科    職種   准教授
論文種別	原著
言語種別	英語
査読の有無	査読あり
表題	Angiotensin II type 1a receptor loss ameliorates chronic tubulointerstitial damage after renal ischemia reperfusion.
掲載誌名	正式名：Scientific reports 略　 称：Sci Rep ISSNコード：045-2322
掲載区分	国外
出版社名	NATURE PUBLISHING GROUP
巻・号・頁	11(1),982頁
著者・共著者	Fujita Y, Ichikawa D, Sugaya T, Ohata K, Tanabe J, Inoue K, Hoshino S, Togo T, Watanabe M, Kimura K, Shibagaki Y, Kamijo-Ikemori A
担当区分	2nd著者
発行年月	2021/01
概要	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.