Regulation of Autophagy in the Heart: 'You Only Live Twice'
| Autor: | James Shaw, Lorrie A. Kirshenbaum, Yaron Aviv, Hongying Gang |
|---|---|
| Rok vydání: | 2011 |
| Předmět: |
Programmed cell death
Physiology Clinical Biochemistry Apoptosis Myocardial Reperfusion Injury Mitochondrion Biology BAG3 Biochemistry Autophagy-Related Protein 5 Stress Physiological Phagosomes Organelle Autophagy Animals Humans Molecular Biology ATG16L1 General Environmental Science Effector Myocardium Cell Biology Cell biology Proto-Oncogene Proteins c-bcl-2 General Earth and Planetary Sciences Signal transduction Microtubule-Associated Proteins |
| Zdroj: | Antioxidants & Redox Signaling. 14:2245-2250 |
| ISSN: | 1557-7716 1523-0864 |
| DOI: | 10.1089/ars.2010.3479 |
| Popis: | Autophagy is a highly orchestrated cellular process by which proteins and organelles are degraded via an elaborate lysosomal pathway to generate free amino acids and sugars for ATP during metabolic stress. At present, the exact role of autophagy in the heart is highly debated but suggested to play a key role in regulating cell turnover in cardiomyopathies and heart failure. The signaling pathways and molecular effectors that govern autophagy are incomplete, as are the mechanisms that determine whether autophagy promotes or prevents cell death. The mitochondrion has been identified as a key organelle centrally involved in regulating autophagy. Certain members of the Bcl-2 gene family, including Beclin-1, Bcl-2 nineteen kilodaltons interacting protein (Bnip3), and Nix/Bnip3L, provoke mitochondrial perturbations leading to permeability transition pore opening, resulting in apoptosis, autophagy, or both. These and other aspects of autophagy processes have been discussed. |
| Databáze: | OpenAIRE |
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