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Editorial
. 2013 Oct 1;305(7):F970-2.
doi: 10.1152/ajprenal.00403.2013. Epub 2013 Jul 17.

Of diabetic mice and ACE2: a new biomarker of renal disease?

Mark C Chappell  1
Affiliations
Editorial

Of diabetic mice and ACE2: a new biomarker of renal disease?

Mark C Chappell. Am J Physiol Renal Physiol. .
No abstract available

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Figures

Fig. 1.
Fig. 1.
Potential scheme for the interaction of ACE2 and ADAMs on the apical surface of the proximal tubules in the diabetic kidney. ANG II binds to the AT1 receptor (AT1R) and stimulates MAP kinase pathways and production of reactive oxygen species (ROS). ACE2 is anchored to the apical membrane and directly converts ANG II to ANG-(1–7). ANG-(1–7) recognizes the AT7/Mas receptor (AT7R) to antagonize the actions of the ANG II-AT1R by stimulation of protein phosphatases (PTP) and generation of nitric oxide (NO). In the diabetic kidney, increased expression of ADAMs may facilitate the release of ACE2 away from the apical surface to increase local concentrations of ANG II and reduce the levels of ANG-(1–7). ADAMs may also promote the expression of the cytokine TNFα and the growth factors EGF and TGFα. ANG II may also contribute to the increased expression of ADAMs and release of EGF. Glc, glucose; Alb, albumin; AGEs, advanced glycated end products.
See this image and copyright information in PMC

Comment on

  • Regulation of urinary ACE2 in diabetic mice.
    Wysocki J, Garcia-Halpin L, Ye M, Maier C, Sowers K, Burns KD, Batlle D. Wysocki J, et al. Am J Physiol Renal Physiol. 2013 Aug 15;305(4):F600-11. doi: 10.1152/ajprenal.00600.2012. Epub 2013 Jun 12. Am J Physiol Renal Physiol. 2013. PMID: 23761674 Free PMC article.

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