Targeting metabolism in cellular senescence, a role for intervention
| Autor: | Christian Sell, Timothy Nacarelli |
|---|---|
| Rok vydání: | 2017 |
| Předmět: |
0301 basic medicine
Senescence Aging Cell cycle checkpoint Cell Cycle Proteins Mechanistic Target of Rapamycin Complex 1 Biology Mitochondrion Biochemistry 03 medical and health sciences Methionine Endocrinology Animals Humans Molecular Biology Cellular Senescence PI3K/AKT/mTOR pathway Sirolimus Metabolism Phenotype Mitochondria Cell biology Glucose 030104 developmental biology Electron Transport Chain Complex Proteins Gene Expression Regulation Cytokines Signal transduction Function (biology) Signal Transduction |
| Zdroj: | Molecular and Cellular Endocrinology. 455:83-92 |
| ISSN: | 0303-7207 |
| Popis: | Cellular senescence has gained much attention as a contributor to aging and susceptibility to disease. Senescent cells undergo a stable cell cycle arrest and produce pro-inflammatory cytokines. However, an additional feature of the senescence phenotype is an altered metabolic state. Despite maintaining a non-dividing state, senescent cells display a high metabolic rate. Metabolic changes characteristic of replicative senescence include altered mitochondrial function and perturbations in growth signaling pathways, such as the mTORC1-signaling pathway. Recent evidence has raised the possibility that these metabolic changes may be essential for the induction and maintenance of the senescent state. Interventions such as rapamycin treatment and methionine restriction impact key aspects of metabolism and delay cellular senescence to extend cellular lifespan. Here, we review the metabolic changes and potential metabolic regulators of the senescence program. In addition, we will discuss how lifespan-extending regimens prevent metabolic stress that accompanies and potentially regulates the senescence program. |
| Databáze: | OpenAIRE |
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