Connecting aging biology and inflammation in the omics era

Aging is characterized by the accumulation of damage to macromolecules and cell architecture that triggers a proinflammatory state in blood and solid tissues, termed inflammaging. Inflammaging has been implicated in the pathogenesis of many age-associated chronic diseases as well as loss of physical...

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Vydané v:The Journal of clinical investigation Ročník 132; číslo 14
Hlavní autori: Walker, Keenan A., Basisty, Nathan, Wilson, David M., Ferrucci, Luigi
Médium: Journal Article
Jazyk:English
Vydavateľské údaje: United States American Society for Clinical Investigation 15.07.2022
Predmet:
Aging
Aging - genetics
Analysis
Biology
Cells
Cellular Senescence - physiology
DNA Damage
Humans
Inflammation
Inflammation - pathology
Mitochondria
Physiological aspects
Review Series
Risk factors
United States
ISSN:1558-8238, 0021-9738, 1558-8238
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Popis
Shrnutí:Aging is characterized by the accumulation of damage to macromolecules and cell architecture that triggers a proinflammatory state in blood and solid tissues, termed inflammaging. Inflammaging has been implicated in the pathogenesis of many age-associated chronic diseases as well as loss of physical and cognitive function. The search for mechanisms that underlie inflammaging focused initially on the hallmarks of aging, but it is rapidly expanding in multiple directions. Here, we discuss the threads connecting cellular senescence and mitochondrial dysfunction to impaired mitophagy and DNA damage, which may act as a hub for inflammaging. We explore the emerging multi-omics efforts that aspire to define the complexity of inflammaging - and identify molecular signatures and novel targets for interventions aimed at counteracting excessive inflammation and its deleterious consequences while preserving the physiological immune response. Finally, we review the emerging evidence that inflammation is involved in brain aging and neurodegenerative diseases. Our goal is to broaden the research agenda for inflammaging with an eye on new therapeutic opportunities.
Bibliografia:ObjectType-Article-1
SourceType-Scholarly Journals-1
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ObjectType-Review-3
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Authorship note: KAW and NB contributed equally to this work.
ISSN:1558-8238
0021-9738
1558-8238
DOI:10.1172/JCI158448