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lüll Autophagic degeneration and death of cardiomyocytes in heart failure Takemura G; Miyata S; Kawase Y; Okada H; Maruyama R; Fujiwara HAutophagy 2006[Jul]; 2 (3): 212-4Numerous cardiomyocytes were found to show autophagic vacuolar degeneration in the UM-X7.1 hamster model of human dilated cardiomyopathy, and autophagy-related proteins--i.e., ubiquitin, cathepsin D and Rab7--were upregulated in those hearts. Importantly, Evans blue-positive cardiomyocytes with leaky plasma membranes were also positive for cathepsin D, suggesting a link between autophagic degeneration and cell death. Treatment with granulocyte colony-stimulating factor (G-CSF) significantly improved survival, cardiac function and remodeling in these animals, and such beneficial effects were accompanied by a reduction in autophagy, an increase in cardiomyocyte size, and a reduction in myocardial fibrosis. G-CSF-induced changes in molecular signaling included activation of Akt and Stat3 (signal transducer and activator of transcription-3), a reduction in the level of myocardial tumor necrosis factor-alpha, and an increase in those of matrix metalloproteinases. In contrast, neither cardiomyocyte apoptosis nor regeneration of cardiomyocytes from bone marrow-derived cells was significant. It thus appears that autophagic death and autophagy-dependent degeneration are important contributors to loss of cardiomyocyte function in the cardiomyopathic hamster and that G-CSF exerts a beneficial effect, mainly via an anti-autophagic mechanism.|Animals[MESH]|Apoptosis/*physiology[MESH]|Autophagy/*physiology[MESH]|Cardiomyopathy, Dilated/pathology[MESH]|Cricetinae[MESH]|Granulocyte Colony-Stimulating Factor/physiology[MESH]|Heart Failure/etiology/*pathology[MESH]|Humans[MESH]|Models, Biological[MESH]|Myocytes, Cardiac/*pathology[MESH] |