Skeletal muscle-specific inducible AMPKα1/α2 knockout mice develop muscle weakness, glycogen depletion, and fibrosis that persists during disuse atrophy
Jonathan J. Petrocelli, Jingtong Liu, Elena M. Yee, Patrick J. Ferrara, Paul‐Emile Bourrant, Naomi M. M. P. de Hart, Sean M. Tatum, W. J. Holland, Katsuhiko Funai, Micah J. Drummond
Abstract
We determined that skeletal muscle-specific AMPKα knockout (KO) mice display functional, fibrotic, and transcriptional alterations before and during muscle disuse atrophy. We also observed that AMPKα KO drives muscle fibrosis and pathways related to cellular senescence that continues during the hindlimb unloading period.
Topics & Concepts
AMPKSkeletal muscleEndocrinologyInternal medicineMuscle atrophyAMP-activated protein kinaseMyocyteBiologyProtein kinase ACell biologyPhosphorylationMedicineMuscle Physiology and DisordersMetabolism, Diabetes, and CancerParkinson's Disease Mechanisms and Treatments