Abstract
AMP-activated kinase (AMPK) is a serine/threonine kinase that is expressed in most cells and activated by a high cellular AMP/ATP ratio (indicating energy deficiency) or by Ca2+. In general, AMPK turns on energy-generating pathways (e.g., glucose uptake, glycolysis, fatty acid oxidation) and stops energy-consuming processes (e.g., lipogenesis, glycogenesis), thereby helping cells survive low energy states. The functional element of the kidney, the nephron, consists of the glomerulus, where the primary urine is filtered, and the proximal tubule, Henle’s loop, the distal tubule, and the collecting duct. In the tubular system of the kidney, the composition of primary urine is modified by the reabsorption and secretion of ions and molecules to yield final excreted urine. The underlying membrane transport processes are mainly energy-consuming (active transport) and in some cases passive. Since active transport accounts for a large part of the cell’s ATP demands, it is an important target for AMPK. Here, we review the AMPK-dependent regulation of membrane transport along nephron segments and discuss physiological and pathophysiological implications.
Highlights
The 5 -adenosine monophosphate (AMP)–activated protein kinase (AMPK) is a serine/threonine protein kinase that is evolutionarily conserved and functions as an intracellular energy sensor in mammalian cells [1,2,3,4,5]
Being expressed in most mammalian cells, AMPK is a heterotrimeric protein consisting of a catalytic α (α1 or α2), scaffolding β (β1 or β2), and a regulatory nucleotide-binding γ (γ1, γ2, or γ3) subunit with the expression pattern differing from cell type to cell type [1,2,11,12,13,14]
This review summarizes the contribution of AMPK to the regulation of renal transport and to the final composition of excreted urine
Summary
The 5 -adenosine monophosphate (AMP)–activated protein kinase (AMPK) is a serine/threonine protein kinase that is evolutionarily conserved and functions as an intracellular energy sensor in mammalian cells [1,2,3,4,5] It is a central regulator of energy homeostasis and affects many important cellular functions including growth, differentiation, autophagy, and metabolism [1,2,6]. AMP or ADP binding to the subunit at cystathionine-beta-synthase repeats results in conformational changes that allows for the phosphorylation at Thr172 by LKB1 This results in an enhancement of AMPK activity by >100-fold [1,8,12,15,31,32,33,34,35,36].
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