Publication Date
8-1-2024
Journal
Disease Models & Mechanisms
DOI
10.1242/dmm.050798
PMID
39136185
PMCID
PMC11340815
PubMedCentral® Posted Date
8-13-2024
PubMedCentral® Full Text Version
Post-print
Published Open-Access
yes
Keywords
Animals, AMP-Activated Protein Kinases, Disease Models, Animal, Humans, Mice, Disease, Phosphorylation, AMPK, Cell signaling, Mouse models
Abstract
AMP-activated protein kinase (AMPK) is an evolutionarily conserved serine/threonine kinase that monitors the cellular energy status to adapt it to the fluctuating nutritional and environmental conditions in an organism. AMPK plays an integral part in a wide array of physiological processes, such as cell growth, autophagy and mitochondrial function, and is implicated in diverse diseases, including cancer, metabolic disorders, cardiovascular diseases and neurodegenerative diseases. AMPK orchestrates many different physiological outcomes by phosphorylating a broad range of downstream substrates. However, the importance of AMPK-mediated regulation of these substrates in vivo remains an ongoing area of investigation to better understand its precise role in cellular and metabolic homeostasis. Here, we provide a comprehensive overview of our understanding of the kinase function of AMPK in vivo, as uncovered from mouse models that harbor phosphorylation mutations in AMPK substrates. We discuss some of the inherent limitations of these mouse models, highlight the broader implications of these studies for understanding human health and disease, and explore the valuable insights gained that could inform future therapeutic strategies for the treatment of metabolic and non-metabolic disorders.
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