Please use this identifier to cite or link to this item: http://hdl.handle.net/1942/40389
Full metadata record
DC FieldValueLanguage
dc.contributor.authorWalker, KA-
dc.contributor.authorBasisty, N-
dc.contributor.authorWILSON, David-
dc.contributor.authorFerrucci, L-
dc.date.accessioned2023-06-14T08:33:12Z-
dc.date.available2023-06-14T08:33:12Z-
dc.date.issued2022-
dc.date.submitted2023-06-07T13:54:16Z-
dc.identifier.citationThe Journal of Clinical Investigation, 132 (14) (Art N° e158448)-
dc.identifier.issn0021-9738-
dc.identifier.urihttp://hdl.handle.net/1942/40389-
dc.description.abstractAging 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.-
dc.description.sponsorshipThis work was supported by the National Institutes of Health (NIH) and the Intramural Research Program, National Institute on Aging (NIA). NB was supported by Longevity Impetus Grants and the Office of Dietary Supplements Scholars Program. We thank Brigit Sullivan, NIH Library Editing Service.-
dc.language.isoen-
dc.publisherAMER SOC CLINICAL INVESTIGATION INC-
dc.rights2022, Walker et al. This is an open access article published under the terms of the Creative Commons Attribution 4.0 International License.-
dc.subject.otherBiology-
dc.subject.otherCellular Senescence-
dc.subject.otherDNA Damage-
dc.subject.otherHumans-
dc.subject.otherAging-
dc.subject.otherInflammation-
dc.titleConnecting aging biology and inflammation in the omics era-
dc.typeJournal Contribution-
dc.identifier.issue14-
dc.identifier.volume132-
local.format.pages13-
local.bibliographicCitation.jcatA1-
local.publisher.place2015 MANCHESTER RD, ANN ARBOR, MI 48104 USA-
local.type.refereedRefereed-
local.type.specifiedReview-
local.bibliographicCitation.artnre158448-
dc.identifier.doi10.1172/jci158448-
dc.identifier.pmid35838044-
dc.identifier.isi000844140900005-
dc.identifier.eissn1558-8238-
local.provider.typeWeb of Science-
local.uhasselt.internationalyes-
item.contributorWalker, KA-
item.contributorBasisty, N-
item.contributorWILSON, David-
item.contributorFerrucci, L-
item.fullcitationWalker, KA; Basisty, N; WILSON, David & Ferrucci, L (2022) Connecting aging biology and inflammation in the omics era. In: The Journal of Clinical Investigation, 132 (14) (Art N° e158448).-
item.accessRightsOpen Access-
item.fulltextWith Fulltext-
item.validationecoom 2023-
crisitem.journal.issn0021-9738-
crisitem.journal.eissn1558-8238-
Appears in Collections:Research publications
Files in This Item:
File Description SizeFormat 
158448.1-20220624181647-covered-e0fd13ba177f913fd3156f593ead4cfd.pdfPublished version3.63 MBAdobe PDFView/Open
Show simple item record

Google ScholarTM

Check

Altmetric


Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.