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Targeting metabolism in cellular senescence, a role for intervention
Journal article   Peer reviewed

Targeting metabolism in cellular senescence, a role for intervention

Timothy Nacarelli and Christian Sell
Molecular and cellular endocrinology, v 455(C), pp 83-92
05 Nov 2017
DOI: https://doi.org/10.1016/j.mce.2016.08.049
PMID: 27591812
Featured in Collection :   UN Sustainable Development Goals @ Drexel

Abstract

Aging - drug effects Aging - genetics Aging - metabolism Animals Cell Cycle Proteins - genetics Cell Cycle Proteins - metabolism Cellular Senescence - drug effects Cellular Senescence - genetics Cytokines - genetics Cytokines - metabolism Electron Transport Chain Complex Proteins - genetics Electron Transport Chain Complex Proteins - metabolism Gene Expression Regulation Glucose - metabolism Humans Mechanistic Target of Rapamycin Complex 1 - antagonists & inhibitors Mechanistic Target of Rapamycin Complex 1 - genetics Mechanistic Target of Rapamycin Complex 1 - metabolism Methionine - administration & dosage Methionine - deficiency Mitochondria - drug effects Mitochondria - genetics Mitochondria - metabolism Phenotype Signal Transduction Sirolimus - pharmacology
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.

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50 citations in Web of Science
53 citations in Scopus

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UN Sustainable Development Goals (SDGs)

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Web of Science research areas
Cell Biology
Endocrinology & Metabolism
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