Key result
Collecting duct (pro)renin receptor promotes renovascular hypertension and ischemic nephropathy in mice.
Why the study?
Nonspecific targeting of the RAS in renovascular hypertension and ischemic nephropathy is only partially effective and limited by hyperkalemia and acute decline of renal function.
May support selective CD PRR inhibition for intrarenal RAS; leaves open clinical translation in renovascular hypertension.
Nonspecifically targeting the RAS in renovascular hypertension and ischemic nephropathy is only partially effective and also limited by class toxicities of hyperkalemia and acute decline of renal function. Our results help understand the CD PRR-mediated local mechanism in the pathogenesis of renovascular hypertension and ischemic nephropathy, and also support CD PRR as a potential therapeutic target for selective inhibition of the intrarenal RAS to treat this devastating disease.
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Fu et al. (2025) studied Renovascular hypertension and ischemic nephropathy. Collecting duct-derived (pro)renin receptor (CD PRR) was evaluated. Collecting duct-derived (pro)renin receptor contributes to the pathogenesis of renovascular hypertension and ischemic nephropathy in mice, highlighting it as a potential therapeutic target.
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