Related Experiment Video
Updated: May 27, 2026

In Situ Immunofluorescent Staining of Autophagy in Muscle Stem Cells
Published on: June 12, 2017
Glycogen synthase kinase-3β controls autophagy during myocardial ischemia and reperfusion
Peiyong Zhai1, Junichi Sadoshima
1Department of Cell Biology and Molecular Medicine, University of Medicine and Dentistry of New Jersey, Newark, NJ, USA.
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.
Related Concept Videos
PI3K/mTOR/AKT Signaling Pathway
Autophagy
An autophagic pathway consists of a series of signaling events activated in response to diverse stress and physiological conditions such as food deprivation,...
Autophagic Cell Death
Autophagy and Apoptosis
Autophagy can activate apoptosis. In normal conditions, the autophagy activating protein Beclin-1 and pro-apoptotic...
Cardiomyopathy III: Hypertrophic Cardiomyopathy
cAMP-dependent Protein Kinase Pathways
Cellular Injury V: Apoptosis and Autophagy
