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Review
. 2019 Sep 3;39(9):BSR20181994.
doi: 10.1042/BSR20181994. Print 2019 Sep 30.

AMPK: a balancer of the renin-angiotensin system

Jia Liu  1   2 , Xuan Li  3 , Qingguo Lu  3 , Di Ren  2 , Xiaodong Sun  3 , Thomas Rousselle  3 , Ji Li  2 , Jiyan Leng  4
Affiliations
Review

AMPK: a balancer of the renin-angiotensin system

Jia Liu et al. Biosci Rep. .

Abstract

The renin-angiotensin system (RAS) is undisputedly well-studied as one of the oldest and most critical regulators for arterial blood pressure, fluid volume, as well as renal function. In recent studies, RAS has also been implicated in the development of obesity, diabetes, hyperlipidemia, and other diseases, and also involved in the regulation of several signaling pathways such as proliferation, apoptosis and autophagy, and insulin resistance. AMP-activated protein kinase (AMPK), an essential cellular energy sensor, has also been discovered to be involved in these diseases and cellular pathways. This would imply a connection between the RAS and AMPK. Therefore, this review serves to draw attention to the cross-talk between RAS and AMPK, then summering the most recent literature which highlights AMPK as a point of balance between physiological and pathological functions of the RAS.

Keywords: ACE; AMPK; Ang II; RAS.

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Conflict of interest statement

The authors declare that there are no competing interests associated with the manuscript.

Figures

Figure 1
Figure 1. The overview of RAS cascade
Abbreviations: AP, aminopeptidase; APA, aminopeptidase A; APN, aminopeptidase N; DCase, decarboxylase; PCP, prolyl carboxy endopeptidase; NEP, neutral endopeptidase; PEP, prolyl endopeptidase; MrgD, Mas-related G-protein-coupled receptor D.
Figure 2
Figure 2. Schematic representation of RAS modulation following AMPK activation
When the RAS is activated, the balance between the classical RAS arm (ACE/AngII/AT1R, red frame) and the protective arm (ACE2/Ang 1-7/MasR, green frame) is broken, thus the pathological changes of the body are induced and concentrated. At this situation, when the AMPK activator is given, the expression of ACE and AT1R are suppressed, while the expression of ACE2 and MasR are increased. At the same time, the up-regulated ACE2 increases the metabolism of AngII to Angl-7, thus activation of AMPK inhibits the classical RAS pathway, and elevation of the RAS protection arm, which keeps the RAS balance.
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References

    1. Li X.C., Zhang J. and Zhuo J.L. (2017) The vasoprotective axes of the renin-angiotensin system: Physiological relevance and therapeutic implications in cardiovascular, hypertensive and kidney diseases. Pharmacol. Res. 125, 21–38 10.1016/j.phrs.2017.06.005 - DOI - PMC - PubMed
    1. Peach M.J. (1977) Renin-angiotensin system: biochemistry and mechanisms of action. Physiol. Rev. 57, 313–370 10.1152/physrev.1977.57.2.313 - DOI - PubMed
    1. Richey J.M., Ader M., Moore D. and Bergman R.N. (1999) Angiotensin II induces insulin resistance independent of changes in interstitial insulin. Am. J. Physiol. 277, E920–E926 - PubMed
    1. Diamond-Stanic M.K. and Henriksen E.J. (2010) Direct inhibition by angiotensin II of insulin-dependent glucose transport activity in mammalian skeletal muscle involves a ROS-dependent mechanism. Arch. Physiol. Biochem. 116, 88–95 10.3109/13813451003758703 - DOI - PMC - PubMed
    1. Zhong J., Guo D., Chen C.B., Wang W., Schuster M., Loibner H.. et al. (2011) Prevention of angiotensin II-mediated renal oxidative stress, inflammation, and fibrosis by angiotensin-converting enzyme 2. Hypertension 57, 314–322 10.1161/HYPERTENSIONAHA.110.164244 - DOI - PubMed

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