Glycogen synthase kinase-3β controls autophagy during myocardial ischemia and reperfusion

Research output: Contribution to journalShort survey

20 Citations (Scopus)

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.

Original languageEnglish (US)
Pages (from-to)138-139
Number of pages2
JournalAutophagy
Volume8
Issue number1
DOIs
StatePublished - Jan 2012

Fingerprint

Glycogen Synthase Kinase 3
Myocardial Reperfusion
Autophagy
Myocardial Ischemia
Ischemia
Reperfusion
Organelles
Protein-Serine-Threonine Kinases
Starvation
Quality Control
Cell Survival
Proteins
Cell Death
Up-Regulation
Heart Failure
Maintenance
Food

All Science Journal Classification (ASJC) codes

  • Molecular Biology
  • Cell Biology

Keywords

  • Autophagy
  • GSK-3β
  • Heart
  • Ischemia
  • Reperfusion
  • mTOR

Cite this

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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.",
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Glycogen synthase kinase-3β controls autophagy during myocardial ischemia and reperfusion. / Zhai, Peiyong; Sadoshima, Junichi.

In: Autophagy, Vol. 8, No. 1, 01.2012, p. 138-139.

Research output: Contribution to journalShort survey

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AB - 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.

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