Autophagy, senescence and apoptosis are tightly linked processes which together determine the fate of cells in response to various stresses. There is ample evidence supporting the notion that senescent cells are highly dependent on autophagy and this process is here much more intensive than in nonsenescent cells. Autophagy may to some extent compensate increased energetic and metabolic demands of senescent cells and also helps with removal of toxic products such as oxidized proteins, protein aggregates and damaged organelles resulting from an overloaded metabolism of some senescent cells. In addition, some studies reported the need of autophagy for the adoption of senescent phenotype. However, there are also studies with seemingly contradictory results claiming that increased autophagy prevents or delays cellular senescence. Relationship of autophagy to apoptosis is similarly ambivalent. Whereas intact autophagy is necessary for the cell, while slightly increased autophagy still has a rather positive impact, excessive autophagy may lead to degradation of critical components necessary for cell function and survival and can trigger one of the modes of programmed cell death. In the first part of this work, we focused on the analysis of autophagic response in senescent and proliferating pancreatic...
| Identifer | oai:union.ndltd.org:nusl.cz/oai:invenio.nusl.cz:337138 |
| Date | January 2014 |
| Creators | Pešina, František |
| Contributors | Anděra, Ladislav, Rudolf, Emil |
| Source Sets | Czech ETDs |
| Language | English |
| Detected Language | English |
| Type | info:eu-repo/semantics/masterThesis |
| Rights | info:eu-repo/semantics/restrictedAccess |
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