About: CD4(+) T Cells at the Center of Inflammaging

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About: CD4(+) T Cells at the Center of Inflammaging Goto Sponge NotDistinct Permalink

An Entity of Type : schema:ScholarlyArticle, within Data Space : covidontheweb.inria.fr associated with source document(s)

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	CD4(+) T Cells at the Center of Inflammaging
Creator	Kroemer, Guido Zitvogel, Laurence
Source	Elsevier; Medline; PMC
abstract	Bharath et al., 2020 report that CD4(+) T lymphocytes from aged individuals exhibit defective mitochondrial autophagy, resulting in altered redox metabolism and upregulation of TH17 cytokines, which in turn may contribute to aging-associated chronic inflammation or “inflammaging.” Of note, the antiaging drug metformin reverses this autophagy defect and rejuvenates CD4(+) T cell function.
has issue date	2020-05-12(xsd:dateTime)
bibo:doi	10.1016/j.cmet.2020.04.016
bibo:pmid	32402265
has license	no-cc
sha1sum (hex)	b02d34a3e126f2abb48e9f412c9573480ea77781
schema:url	https://doi.org/10.1016/j.cmet.2020.04.016
resource representing a document's title	CD4(+) T Cells at the Center of Inflammaging
has PubMed Central identifier	PMC7217078
has PubMed identifier	32402265
schema:publication	Cell Metab
resource representing a document's body	covid:b02d34a3e126f2abb48e9f412c9573480ea77781#body_text
is schema:about of	named entity 'CD4 +' named entity 'Inflammaging' named entity 'mitochondrial' named entity 'Tempol' named entity 'metabolism' named entity 'antiaging' named entity 'preclinical' named entity 'cytokines' named entity 'Metformin' named entity 'autophagic' named entity 'metformin' named entity 'autophagy' named entity 'inflammaging' named entity 'autophagy' named entity 'gene' named entity 'reactive oxygen species' named entity 'CD4 +' named entity 'mitophagy' named entity 'STAT3' named entity 'age-related' named entity 'metformin' named entity 'lymphocytes' named entity 'TH17' named entity 'TH17' named entity 'obesity' named entity 'vicious cycle' named entity 'cytoplasm' named entity 'IL-23' named entity 'Tocilizumab' named entity 'metformin' named entity 'phenotype' named entity 'metformin' named entity 'ATG3' named entity 'phenotype' named entity 'endoplasmic reticulum' named entity 'biomarkers' named entity 'microbiota' named entity 'oral antidiabetic' named entity 'IL-6 receptor' named entity 'CD4 +' named entity 'inflammatory reactions' named entity 'Bharath' named entity 'metformin' named entity 'autophagy' named entity 'CD4 +' named entity 'TH17' named entity 'phosphorylation' named entity 'mitochondrial' named entity 'Bharath' named entity 'cell types' named entity 'metformin' named entity 'CD4 +' named entity 'inflammaging' named entity 'CD4 +' named entity 'COVID-19' named entity 'autophagy' named entity 'TH17' named entity 'cell receptors' named entity 'biological age' named entity 'metformin' named entity 'inflammatory responses' named entity 'Metformin' named entity 'radical scavenger' named entity 'autophagy' named entity 'pharmacological' named entity 'siRNA' named entity 'Bharath' named entity 'autophagy' named entity 'CD4 +' named entity 'Bharath' named entity 'COVID-19' named entity 'phenotype' named entity 'inflammation' named entity 'phenotype' named entity 'inflammation' named entity 'pro-inflammatory' named entity 'IL17A' named entity 'aging process' named entity 'TH17' named entity 'NLRP3'

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