The role of autophagy in cardiomyocytes in the basal state and in response to hemodynamic stress

By Atsuko Nakai, O. Yamaguchi, Toshihiro Takeda, Y. Higuchi, S. Hikoso, M. Taniike, S. Omiya, Isamu Mizote, Y. Matsumura, M. Asahi and 4 more. Nature Medicine, 2007

1,518 citations recorded by the source corpus.

Subfields: Cell Biology, Epidemiology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/a715cda372c5ad70240b5a892d5f0be6fb6256d0

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Citations in the corpus

Autophagy: a lysosomal degradation pathway with a central role in health and disease. (2009, background): “autophagy protein Atg5 causes cardiomyopathy inmice [86].”
A role for the NAD-dependent deacetylase Sirt1 in the regulation of autophagy (2008, background): “Recent evidence suggests that the accumulation of p62 represents a convenient in vivo marker for impaired autophagy (16, 17).”
Autophagy: process and function. (2007, background): “Likewise, autophagy is suggested to be a protective response in cardiomyocytes during hemodynamic stress, but the mechanisms remain to be elucidated (Nakai et al. 2007).”
Autophagy is important in islet homeostasis and compensatory increase of beta cell mass in response to high-fat diet. (2008, background): “…constitutive autophagy is also important for maintaining the quality of proteins and organelles, in order to maintain cell functions, as recently reported in various organs, including the liver (Komatsu et al., 2005), brain (Hara et al., 2006; Komatsu et al., 2006), and heart (Nakai et al., 2007).”
Pathophysiology of cardiac hypertrophy and heart failure: signaling pathways and novel therapeutic targets (2015, background): “Regulation of key autophagy proteins (Atg5 and Atg7) in the heart using genetic mouse models suggest that autophagy protects against pathological remodeling and contractile dysfunction (Bhuiyan et al. 2013; Nakai et al. 2007).”
Autophagy and Mitophagy in Cardiovascular Disease. (2017, background): “Mice subjected to the temporally controlled cardiomyocyte-specific deletion of Atg5 (autophagy related 5)—which is required for optimal autophagic responses(4)—developed cardiac hypertrophy, left ventricular dilatation, contractile dysfunction, and premature death accompanied by disorganized sarcome”
Autophagy is required to maintain muscle mass. (2009, positive): “…from one to the next Z line, presence of swollen mitochondria, sarcoplasmic reticulum distension, and formation of aberrant concentric membranous structure (Figures 2F and S13) similar to those observed in Atg7-deficient livers and Atg5-deficient hearts (Komatsu et al., 2005; Nakai et al., 2007).”
Cellular Stress Responses: Cell Survival and Cell Death (2010, background): “Although it is still controversial whether autophagy is protective or toxic for the cells, accumulating evidence suggests that it has beneficial roles in the heart under both physiological and pathological conditions [45, 46].”