title: Glycogen synthase kinase-3β controls autophagy during myocardial ischemia and reperfusion.
abstract: Autophagy is a catabolic process that degrades long-lived proteins, pathogens and damaged organelles. Autophagy is active in the heart at baseline and is further stimulated by stresses, such as nutrient starvation, ischemia/reperfusion (I/R) and heart failure. Baseline autophagy plays an adaptive role in the heart, and contributes to the maintenance of cardiac structure and function and the inhibition of age-associated abnormalities, by achieving quality control of proteins and organelles. Activation of autophagy during ischemia is beneficial because it improves cell survival and cardiac function. However, excessive autophagy with robust upregulation of BECN1 during reperfusion appears to enhance cell death, which is detrimental to the heart. We have shown recently that autophagy during prolonged ischemia and I/R is critically regulated by glycogen synthase kinase-3β (GSK-3β), a ubiquitously expressed serine/threonine kinase, in a phase-dependent manner. Here we discuss the role of GSK-3β in mediating autophagy in the heart.
authors: Department of Cell Biology and Molecular Medicine, University of Medicine and Dentistry of New Jersey, Newark, NJ, USA.
authors: Peiyong
authors: P
authors: Zhai
authors: Junichi
authors: J
authors: Sadoshima
mesh_terms: D001343:Autophagy; D038362:Glycogen Synthase Kinase 3 / Q000378:metabolism*; D000071679:Glycogen Synthase Kinase 3 beta; D006801:Humans; D015428:Myocardial Reperfusion Injury / Q000201:enzymology* / Q000473:pathology*; D058570:TOR Serine-Threonine Kinases / Q000378:metabolism
chemical_list: C000605506:GSK3B protein, human; D000071679:Glycogen Synthase Kinase 3 beta; D058570:TOR Serine-Threonine Kinases; D038362:Glycogen Synthase Kinase 3