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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Veröffentlicht in:The Journal of clinical investigation Jg. 132; H. 14
Hauptverfasser: Walker, Keenan A., Basisty, Nathan, Wilson, David M., Ferrucci, Luigi
Format: Journal Article
Sprache:Englisch
Veröffentlicht: United States American Society for Clinical Investigation 15.07.2022
Schlagworte:
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
Online-Zugang:Volltext
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Abstract 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.
AbstractList 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.
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.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.
Audience Academic
Author Basisty, Nathan
Wilson, David M.
Ferrucci, Luigi
Walker, Keenan A.
AuthorAffiliation 2 Biomedical Research Institute, Faculty of Medicine and Life Sciences, Hasselt University, Diepenbeek, Belgium
1 Intramural Research Program of the National Institute on Aging, NIH, Baltimore, Maryland, USA
AuthorAffiliation_xml – name: 1 Intramural Research Program of the National Institute on Aging, NIH, Baltimore, Maryland, USA
– name: 2 Biomedical Research Institute, Faculty of Medicine and Life Sciences, Hasselt University, Diepenbeek, Belgium
Author_xml – sequence: 1
  givenname: Keenan A.
  orcidid: 0000-0002-5989-9853
  surname: Walker
  fullname: Walker, Keenan A.
– sequence: 2
  givenname: Nathan
  orcidid: 0000-0001-6173-1139
  surname: Basisty
  fullname: Basisty, Nathan
– sequence: 3
  givenname: David M.
  orcidid: 0000-0002-8945-0395
  surname: Wilson
  fullname: Wilson, David M.
– sequence: 4
  givenname: Luigi
  surname: Ferrucci
  fullname: Ferrucci, Luigi
BackLink https://www.ncbi.nlm.nih.gov/pubmed/35838044$$D View this record in MEDLINE/PubMed
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Snippet Aging is characterized by the accumulation of damage to macromolecules and cell architecture that triggers a proinflammatory state in blood and solid tissues,...
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proquest
gale
pubmed
crossref
SourceType Open Website
Open Access Repository
Aggregation Database
Index Database
Enrichment Source
SubjectTerms Aging
Aging - genetics
Analysis
Biology
Cells
Cellular Senescence - physiology
DNA Damage
Humans
Inflammation
Inflammation - pathology
Mitochondria
Physiological aspects
Review Series
Risk factors
Title Connecting aging biology and inflammation in the omics era
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Volume 132
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