Advanced glycation end-products induce skeletal muscle atrophy and dysfunction in diabetic mice via a RAGE-mediated, AMPK-down-regulated, Akt pathway - Chiu, Chen-Yuan; Yang, Rong-Sen; Sheu, Meei-Ling; Chan, Ding-Cheng; Yang, Ting-Hua; Tsai, Keh-Sung; Chiang, Chih-Kang; Liu, Shing-Hwa (The Journal of pathology, 2016)
Keywords: advanced glycation end-products; Aged; alagebrium chloride; AMP-Activated Protein Kinases - metabolism; Animals; Atrophy - etiology; Atrophy - pathology; Case-Control Studies; Diabetes Mellitus - etiology; Diabetes Mellitus, Experimental - etiology; diabetic myopathy; Down-Regulation; Glycation End Products, Advanced - metabolism; Humans; Male; MAP Kinase Signaling System - physiology; Mice; Muscle Fatigue - physiology; Muscle Fibers, Skeletal - pathology; Muscle Proteins - metabolism; Muscle Weakness - etiology; Muscle Weakness - pathology; Muscle, Skeletal - pathology; Muscle, Skeletal - physiology; Muscular Diseases - etiology; Muscular Diseases - pathology; Receptor for Advanced Glycation End Products - physiology; Regeneration - physiology; Signal Transduction - physiology; SKP Cullin F-Box Protein Ligases - metabolism; Thiazoles - pharmacology; alagebrium chloride; diabetic myopathy; advanced glycation end-products