Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The . gov means it’s official. Federal government websites often end in . gov or VSports app下载. mil. Before sharing sensitive information, make sure you’re on a federal government site. .

Https

The site is secure V体育官网. The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely. .

Review
. 2015 Apr 21:6:117.
doi: 10.3389/fphys.2015.00117. eCollection 2015.

Role of non-classical renin-angiotensin system axis in renal fibrosis

Lin-Li Lv  1 , Bi-Cheng Liu  1
Affiliations
Review

Role of non-classical renin-angiotensin system axis in renal fibrosis

Lin-Li Lv et al. Front Physiol. .

Abstract

The renin-angiotensin system (RAS) is a major regulator of renal fibrosis. Besides the classical renin/Angiotensin-converting enzyme (ACE)/angiotensin II (Ang II)/AT1 and AT2 axis, multiple new axes have been recently described. The new members have added new dimensions to RAS, including the ACE2/Ang(1-7)/Mas receptor axis, the prorenin/(pro)renin receptor(PRR)/intracelluar pathway axis, and the Angiotensin A (Ang A), alamandine-Mas-related G protein coupled receptor D(MrgD) axis VSports手机版. This review summarized recent studies regarding role of the non-classical RAS axis in renal fibrosis, and its possible implications to the intervention of progression of chronic kidney disease. .

Keywords: (pro)renin; angiotensin(1–7); angiotensin-converting enzyme 2; renal fibrosis; renin-angiotensin system. V体育安卓版.

PubMed Disclaimer

Figures

Figure 1
Figure 1
Schematic representation for the role of new members of RAS system in renal fibrosis and the potential molecules targeted RAS for therapeutic application.
See this image and copyright information in PMC

References

    1. Advani A., Kelly D. J., Cox A. J., White K. E., Advani S. L., Thai K., et al. . (2009). The (Pro)renin receptor: site-specific and functional linkage to the vacuolar H+-ATPase in the kidney. Hypertension 54, 261–269. 10.1161/HYPERTENSIONAHA.109.128645 - DOI - PubMed
    1. Alzayadneh E. M., Chappell M. C. (2014). Angiotensin-(1-7) abolishes AGE-induced cellular hypertrophy and myofibroblast transformation via inhibition of ERK1/2. Cell. Signal. 26, 3027–3035. 10.1016/j.cellsig.2014.09.010 - DOI - PMC - PubMed
    1. Axelband F., Dias J., Miranda F., Ferrao F. M., Barros N. M., Carmona A. K., et al. . (2009). A scrutiny of the biochemical pathways from Ang II to Ang-(3-4) in renal basolateral membranes. Regul. Pept. 158, 47–56. 10.1016/j.regpep.2009.08.004 - DOI - PubMed
    1. Binger K. J., Muller D. N. (2013). Autophagy and the (Pro)renin receptor. Front. Endocrinol. 4:155 10.3389/fendo.2013.00155 - DOI (V体育官网) - PMC - PubMed
    1. Brosnihan K. B., Neves L. A., Chappell M. C. (2005). Does the angiotensin-converting enzyme (ACE)/ACE2 balance contribute to the fate of angiotensin peptides in programmed hypertension? Hypertension 46, 1097–1099. 10.1161/01.HYP.0000185149.56516.0a - "V体育ios版" DOI - PubMed

LinkOut - more resources