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Divergent mechanisms of metabolic dysfunction drive fibroblast and T-cell senescence
Affiliation:1. Laboratory for Neurodegenerative Research, Ann Romney Center for Neurologic Diseases, Brigham and Women''s Hospital and Harvard Medical School, Harvard Institutes of Medicine, Boston, MA, USA;2. Neurobehaviour Laboratory Core, Harvard NeuroDiscovery Center, Boston, MA, USA;3. Department of Molecular, Cellular and Developmental Biology, Neuroscience Research Institute, University of California, Santa Barbara, CA, USA;1. Gerontology Department and Frailty in Aging Research (FRIA) Group, Faculty of Medicine and Pharmacy, Vrije Universiteit Brussel, Laarbeeklaan 103, B-1090 Brussel, Belgium;2. Laboratory of Molecular and Cellular Therapy, Vrije Universiteit Brussel, Laarbeeklaan 103, B-1090 Brussel, Belgium;3. Laboratory of Hematology, Universitair Ziekenhuis Brussel, Laarbeeklaan 101, B-1090 Brussel, Belgium;4. Department of Geriatrics, Universitair Ziekenhuis Brussel, Laarbeeklaan 101, B-1090 Brussel, Belgium;1. Finnish Environment Institute, Natural Environment Centre, Mechelininkatu 34 a, P.O. Box 140, FI-00251 Helsinki, Finland;2. Finnish Museum of Natural History, P.O. Box 17, FI-00014 University of Helsinki, Finland;1. Cooperative Institute for Marine and Atmospheric Studies, Rosenstiel School of Marine & Atmospheric Science, University of Miami, Miami, FL, 33149, USA;2. Fisheries Centre, AERL, 2202 Main Mall, University of British Columbia, Vancouver, BC, V6T 1Z4, Canada
Abstract:
The impact of cellular senescence during ageing is well established, however senescence is now recognised to play a role in a variety of age related and metabolic diseases, such as cancer, autoimmune and cardiovascular diseases. It is therefore crucial to gain a better understanding of the mechanisms that control cellular senescence. In recent years our understanding of the intimate relationship between cell metabolism, cell signalling and cellular senescence has greatly improved. In this review we discuss the differing roles of glucose and protein metabolism in both senescent fibroblast and CD8+ T-cells, and explore the impact cellular metabolism has on the senescence-associated secretory phenotype (SASP) of these cell types.
Keywords:Ageing  T-cell  Fibroblast  Senescence  Metabolism  SASP
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