AMPK: a balancer of the renin–angiotensin system

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.

Metformin and risk of mortality in patients hospitalised with COVID-19: a retrospective cohort analysis

“… 29 Lastly, activation of AMPK by metformin can lead to increased expression of ACE2 and conformational changes to ACE2, and possibly decreased binding of SARS-CoV-2 to the ACE2 receptor. 30 Recent work by Li and colleagues 19 found that expression of the ACE2 receptor was equal in male and female human lungs, but that cytokine responses differed. This difference in subsequent inflammatory response and our sex-specific findings might support the anti-inflammatory effects of metformin as the primary means of benefit in COVID-19.…”

AT1R/GSK-3β/mTOR Signaling Pathway Involved in Angiotensin II-Induced Neuronal Apoptosis after HIE Both In Vitro and In Vivo

“…For example, Wu et al found that Ang II could induce cardiac remodeling [ 38 ]; Fan et al revealed that Ang II promoted capillary damage in cerebral vasculature [ 39 ]. Additionally, Liu et al reported that Ang II was an important mediator in the pathogenesis of diabetes, obesity, and hyperlipidemia and also regulates apoptosis, proliferation, autophagy, and insulin resistance [ 40 ]. Moreover, several studies also revealed that Ang II could increase cerebral hypoperfusion-induced anxiety-like behavior and promote memory impairment [ 41 ], induce neuronal dysfunction [ 42 ], contribute to the pathogenesis of Alzheimer's Disease [ 43 ], cause neuronal damage [ 44 ] hippocampal neural stem cell death, and memory impairment [ 45 ].…”

<p>Emerging Roles and Therapeutic Interventions of Aerobic Glycolysis in Glioma</p>

“…132 The γ subunit serves as an allosteric activator, while the β subunit provides a structural bridge between α and γ subunits. 134,136 Therefore, upon binding to γ-subunit, AMPK would be elevated via the allosteric activation of AMP, which could also be precisely modulated by upstream kinases. 137,138 More importantly, phosphorylating of AMPK signaling depends on adenosine triphosphate ATP/AMP ratio to a great extent.…”