Enhancement of angiotensin II type 1 receptor-associated protein suppresses kidney inflammation in a mouse model of aristolochic acid nephropathy.

ABSTRACT: Chronic kidney disease generally progresses to irreversible fibrosis through chronic inflammation and age-related changes. We had previously reported that genetic knockdown of angiotensin II type 1 receptor (AT1R)-associated protein (ATRAP) exacerbates aging-associated kidney tubulointerstitial fibrosis in mice. However, whether enhanced ATRAP expression can suppress renal fibrosis and senescence in vivo remains unknown. Recently, we proposed that aristolochic acid nephropathy (AAN) could be used for modeling kidney aging with fibrosis. The present study aimed to investigate the functional role of ATRAP in aging-associated kidney fibrosis and inflammation using ATRAP transgenic (Tg19) mice subjected to AAN. AA administration caused histological renal fibrosis and enhanced ATRAP expression

SUBMITTER: Furuta R 

PROVIDER: S-EPMC12314130 | biostudies-literature | 2025 Jul

REPOSITORIES: biostudies-literature