Too much of a good thing is bad: proteasome inhibition induces stressed hearts to fail.

摘要

A fine balance between protein synthesis and protein degradation regulates cellular homeostasis. Cardiac remodelling is a common response of the heart to changes in physiological or pathological demand. Hypertrophic growth is the primary mechanism through which the heart normalizes ventricular wall stress. It is characterized by an increase in the volume of individual cardiac myocytes, which can be the result of an acceleration of synthesis or a reduced degradation rate of proteins. However, while the synthesis rate has always been shown to be increased, protein degradation has been shown to be either accelerated or unchanged in hypertrophic hearts and inhibited by induction of cardiac work or high aortic pressure in Langendorff preparations.