| Autor: |
Ganzleben I; Department of Medicine 1, University Hospital, Friedrich-Alexander-Universität Erlangen-Nürnberg, 91054 Erlangen, Germany.; Deutsches Zentrum Immuntherapie (DZI), Universitätsklinikum Erlangen, 91054 Erlangen, Germany., Neurath MF; Department of Medicine 1, University Hospital, Friedrich-Alexander-Universität Erlangen-Nürnberg, 91054 Erlangen, Germany.; Deutsches Zentrum Immuntherapie (DZI), Universitätsklinikum Erlangen, 91054 Erlangen, Germany., Becker C; Department of Medicine 1, University Hospital, Friedrich-Alexander-Universität Erlangen-Nürnberg, 91054 Erlangen, Germany.; Deutsches Zentrum Immuntherapie (DZI), Universitätsklinikum Erlangen, 91054 Erlangen, Germany. |
| Abstrakt: |
Autophagy is a crucial general survival tactic of mammalian cells. It describes the capability of cells to disassemble and partially recycle cellular components (e.g., mitochondria) in case they are damaged and pose a risk to cell survival or simply if their resources are urgently needed elsewhere at the time. Autophagy-associated pathomechanisms have been increasingly recognized as important disease mechanisms in non-malignant (neurodegeneration, diffuse parenchymal lung disease) and malignant conditions alike. However, the overall consequences of autophagy for the organism depend particularly on the greater context in which autophagy occurs, such as the cell type or whether the cell is proliferating. In cancer, autophagy sustains cancer cell survival under challenging, i.e., resource-depleted, conditions. However, this leads to situations in which cancer cells are completely dependent on autophagy. Accordingly, autophagy represents a promising yet complex target in cancer treatment with therapeutically induced increase and decrease of autophagic flux as important therapeutic principles. |
