Abstract
In albumin overload (AO) nephropathy model, PRR activation mediated activation of intrarenal renin-angiotensin system (RAS) and thus elevated inflammatory and fibrosis factors of the kidney. In the present study, our goal was to determine whether such action of PRR was mediated by PRR soluble form (sPRR), cleaved by site-1 protease (S1P), a serine protease in the Golgi.
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