Regulation of inflammation as an anti‐aging intervention
© 2019 Federation of European Biochemical Societies. Aging is accompanied by a decline in physiological integrity and a loss of regenerative capacity in many tissues. The development of interventions that prevent or reverse age-related disease requires a better understanding of the interplay of cell...
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Published in | The FEBS journal Vol. 287; no. 1; pp. 43 - 52 |
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Main Authors | , |
Format | Journal Article |
Language | English |
Published |
England
John Wiley & Sons, Inc
01.01.2020
Blackwell Publishing Ltd |
Subjects | |
Online Access | Get full text |
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Summary: | © 2019 Federation of European Biochemical Societies.
Aging is accompanied by a decline in physiological integrity and a loss of regenerative capacity in many tissues. The development of interventions that prevent or reverse age-related disease requires a better understanding of the interplay of cell intrinsic, inter-cellular communication and systemic deregulations that underlie the aging process. Immune dysfunction and changes in inflammatory pathways are transversal contributors to the aging process and are essential propagators of tissue deterioration. Here, we propose and discuss the rejuvenation potential of interventions that target chronic inflammation and how modulation of tissue repair capacity could be an important mediator of such anti-aging strategies. We highlight how current knowledge on the systemic nature of inflammatory dysregulation in old organisms, together with the development of new animal models that allow for the isolation of the inflammatory component of aging, could provide new targets for interventions in aging based on the modulation of inflammatory pathways.
JN and PS-V acknowledge support from iMM start-up funding and “la caixa” Foundation for the Junior Leader Fellowship for PS-V (LCF/BQ/PI19/11690006) |
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Bibliography: | ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-3 content type line 23 ObjectType-Review-1 |
ISSN: | 1742-464X 1742-4658 |
DOI: | 10.1111/febs.15061 |