AMPK: guardian of metabolism and mitochondrial homeostasis

Abstract

Cells constantly adapt their metabolism to meet their energy needs and respond to nutrient availability. Eukaryotes have evolved a very sophisticated system to sense low cellular ATP levels via the serine/threonine kinase AMP-activated protein kinase (AMPK) complex. Under conditions of low energy, AMPK phosphorylates specific enzymes and growth control nodes to increase ATP generation and decrease ATP consumption. In the past decade, the discovery of numerous new AMPK substrates has led to a more complete understanding of the minimal number of steps required to reprogramme cellular metabolism from anabolism to catabolism. This energy switch controls cell growth and several other cellular processes, including lipid and glucose metabolism and autophagy. Recent studies have revealed that one ancestral function of AMPK is to promote mitochondrial health, and multiple newly discovered targets of AMPK are involved in various aspects of mitochondrial homeostasis, including mitophagy This Review discusses how AMPK functions as a central mediator of the cellular response to energetic stress and mitochondrial insults and coordinates multiple features of autophagy and mitochondrial biology.

AICAR Prevents Acute Olanzapine-Induced Disturbances in Glucose Homeostasis

“…5A). There were no significant differences in the hypothalamic P-AMPK/AMPK ratio between groups, however there was a main effect of AICAR on the hypothalamic P-ACC/ACC ratio (p=0.033), indicating activation of AMPK (Herzig and Shaw, 2018) (Fig. 5B & C).…”

Resveratrol Modulates Apoptosis and Autophagy Induced by High Glucose and Palmitate in Cardiac Cells

“…AMPK is a serine/threonine kinase that senses cellular energy status and regulates energy homeostasis [31]. Activation of AMPK is involved in determining multiple cellular processes, including cell growth, apoptosis [32], and autophagy [33]. It is known that the activation of AMPK could inhibit mTOR, the best-characterized protein kinase that negatively regulates autophagy [19].…”

Fatty acid metabolism in CD8+ T cell memory: Challenging current concepts

“…Yet, how CD8 + T cells can actively coordinate mTOR activity and thus memory development at the molecular level is still not fully understood. One important negative regulator of mTORC1 that has been associated with T mem cell development is the AMP-activated protein kinase (AMPK) (Figure 1) (recently reviewed in (83, 84)). AMPK is a heterotrimeric serine/threonine protein kinase composed of one catalytic α subunit, and regulatory β and γ subunits that is typically activated under metabolic stress (translated in high AMP and ADP concentrations) and modulates cellular metabolism by inhibiting anabolic and promoting catabolic metabolism (85–89).…”