Abstract
Prorenin binding to the (pro)renin receptor not only causes a nonproteolytic activation of prorenin leading to the activation of the renin-angiotensin system (RAS), but also stimulates the receptor's own intracellular signaling pathways independent of the RAS. Within the kidneys, the (pro)renin receptor is present in the glomerular mesangium and podocytes, which play an important role in the maintenance of the glomerular filtration barrier. Therefore, prorenin-receptor blockers, which competitively bind to the receptor as a decoy peptide, have superior benefits with regard to proteinuria and glomerulosclerosis in experimental animal models with elevated plasma prorenin levels such as diabetes and hypertension compared with conventional RAS inhibitors, possibly by inhibiting both the nonproteolytic activation of prorenin and RAS-independent intracellular signals.
| Original language | English |
|---|---|
| Pages (from-to) | 524-528 |
| Number of pages | 5 |
| Journal | Seminars in Nephrology |
| Volume | 27 |
| Issue number | 5 |
| DOIs | |
| Publication status | Published - 2007 Sep |
Fingerprint
Keywords
- Angiotensin
- mesangium
- nonproteolytic activation
- podocytes
- prorenin
ASJC Scopus subject areas
- Nephrology
Cite this
The (Pro)Renin Receptor and the Kidney. / Ichihara, Atsuhiro; Kaneshiro, Yuki; Takemitsu, Tomoko; Sakoda, Mariyo; Itoh, Hiroshi.
In: Seminars in Nephrology, Vol. 27, No. 5, 09.2007, p. 524-528.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - The (Pro)Renin Receptor and the Kidney
AU - Ichihara, Atsuhiro
AU - Kaneshiro, Yuki
AU - Takemitsu, Tomoko
AU - Sakoda, Mariyo
AU - Itoh, Hiroshi
PY - 2007/9
Y1 - 2007/9
N2 - Prorenin binding to the (pro)renin receptor not only causes a nonproteolytic activation of prorenin leading to the activation of the renin-angiotensin system (RAS), but also stimulates the receptor's own intracellular signaling pathways independent of the RAS. Within the kidneys, the (pro)renin receptor is present in the glomerular mesangium and podocytes, which play an important role in the maintenance of the glomerular filtration barrier. Therefore, prorenin-receptor blockers, which competitively bind to the receptor as a decoy peptide, have superior benefits with regard to proteinuria and glomerulosclerosis in experimental animal models with elevated plasma prorenin levels such as diabetes and hypertension compared with conventional RAS inhibitors, possibly by inhibiting both the nonproteolytic activation of prorenin and RAS-independent intracellular signals.
AB - Prorenin binding to the (pro)renin receptor not only causes a nonproteolytic activation of prorenin leading to the activation of the renin-angiotensin system (RAS), but also stimulates the receptor's own intracellular signaling pathways independent of the RAS. Within the kidneys, the (pro)renin receptor is present in the glomerular mesangium and podocytes, which play an important role in the maintenance of the glomerular filtration barrier. Therefore, prorenin-receptor blockers, which competitively bind to the receptor as a decoy peptide, have superior benefits with regard to proteinuria and glomerulosclerosis in experimental animal models with elevated plasma prorenin levels such as diabetes and hypertension compared with conventional RAS inhibitors, possibly by inhibiting both the nonproteolytic activation of prorenin and RAS-independent intracellular signals.
KW - Angiotensin
KW - mesangium
KW - nonproteolytic activation
KW - podocytes
KW - prorenin
UR - http://www.scopus.com/inward/record.url?scp=34548483245&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=34548483245&partnerID=8YFLogxK
U2 - 10.1016/j.semnephrol.2007.07.005
DO - 10.1016/j.semnephrol.2007.07.005
M3 - Article
VL - 27
SP - 524
EP - 528
JO - Seminars in Nephrology
JF - Seminars in Nephrology
SN - 0270-9295
IS - 5
ER -