Key points are not available for this paper at this time.
Design
Review
S1P inhibition merits exploration for fluid disorders and CKD; leaves open whether targeting alters clinical outcomes.
PURPOSE OF REVIEW: (Pro)renin receptor (PRR) belongs to type I transmembrane receptor family and binds both prorenin and renin, representing a potential regulator of the activity of the renin-angiotensin system. Soluble form of PRR (sPRR) is generated by intracellular protease-mediated cleavage of full-length PRR. The purpose of this review is to highlight recent advances in understanding the mechanisms of action and production of sPRR. RECENT FINDINGS: It has recently been demonstrated that site-1-protease (S1P) plays a dominant role in the generation of sPRR. New evidence is also emerging to support a biological function of sPRR in the physiological regulation of fluid homeostasis as well as pathogenesis of chronic kidney disease. SUMMARY: sPRR is a 28 kDa product of PRR cleavage via S1P-mediated protease activity. Not only does sPRR regulate renal tubular water transport, but it also mediates pathogenic responses to renal cellular injury. sPRR is likely involved in a wide range of physio-pathological processes.
No takes yet. Share an insight, caveat, or question.
Zhu et al. (2018) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: