An expanded role for AMP-activated protein kinase: regulator of myocardial protein degradation.
Rudolph Schoenheimer's concept of the "dynamic state of body constituents" has existed since the 1940s, but the idea that heart muscle cells renew themselves from within is relatively new. Many studies have elucidated the interaction of metabolic pathways for energy provision and contraction of the heart, and work in the field has uncovered novel metabolic regulators of enzyme action. However, the impact of myocardial energy metabolism on myocardial protein turnover has received little attention. Here, we review recent findings that identify metabolic signals as regulators of myocardial protein turnover and seek to broaden the role of energy substrate metabolism from a provider of ATP to a regulator of self-renewal of the cardiomyocyte.
Department of Internal Medicine, Division of Cardiology, The University of Texas Medical School at Houston, Houston, TX 77030, USA.
Kedryn K
KK
Baskin
Heinrich
H
Taegtmeyer
D055372:AMP-Activated Protein Kinases / Q000502:physiology*; D004734:Energy Metabolism / Q000502:physiology; D006801:Humans; D009206:Myocardium / Q000201:enzymology*; D032383:Myocytes, Cardiac / Q000378:metabolism; D059748:Proteolysis
D055372:AMP-Activated Protein Kinases