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Ageing Res Rev. 2018 Nov;47:24-30. doi: 10.1016/j.arr.2018.06.001. Epub 2018 Jun 15.

Divergent mechanisms of metabolic dysfunction drive fibroblast and T-cell senescence.

Author information

1
William Harvey Research Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, Charterhouse Square, London EC1M 6BQ, UK.
2
William Harvey Research Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, Charterhouse Square, London EC1M 6BQ, UK. Electronic address: s.henson@qmul.ac.uk.

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; Fibroblast; Metabolism; SASP; Senescence; T-cell

PMID:
29902528
DOI:
10.1016/j.arr.2018.06.001
[Indexed for MEDLINE]

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