Is intracellular protein aggregation a proximal trigger of cardiomyocyte autophagy?
We conclude that protein aggregation is a proximal trigger of cardiomyocyte autophagy and that autophagic activity functions to attenuate aggregate/aggresome formation in heart. Findings reported here are the first to demonstrate that protein aggregation occurs in response to hemodynamic stress, situating pressure-overload heart disease in the category of proteinopathies.
ILPs did not affect the 1- and 2-year clinical results of patients who sustained these injuries during hip arthroscopy.