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Agingisamajorriskfactorformanydiseases,especiallyinhighlyprevalentcardiopulmonarycomorbiditiesandinfectiousdiseases
includingCoronavirus Disease 2019 (COVID-19).Resolving cellular and molecular mechanisms associated withaging inhigher
mammalsistherefore urgentlyneeded.Here, wecreatedyoung and oldnon-human primatesingle-nucleus/cell transcriptomic
atlasesof lung,heart and artery, thetop tissuestargeted by SARS-CoV-2. Analysis of celltype-specificaging-associated
transcriptional changes revealed increasedsystemic inflammation and compromised virus defense asa hallmark of
cardiopulmonaryaging.Withage,expressionoftheSARS-CoV-2receptorangiotensin-convertingenzyme2(ACE2)wasincreasedin
thepulmonary alveolarepithelial barrier, cardiomyocytes, and vascularendothelial cells.We foundthat interleukin 7(IL7)
accumulated inaged cardiopulmonary tissuesand inducedACE2 expression inhuman vascularendothelial cellsin anNF-κB-
dependentmanner.Furthermore,treatmentwithvitaminCblockedIL7-inducedACE2expression.Altogether,ourfindingsdepict
thefirsttranscriptomicatlasoftheagedprimatecardiopulmonarysystemandprovidevitalinsightsintoage-linkedsusceptibilityto | |
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SARS-CoV-2, suggesting that geroprotective strategies mayreduceCOVID-19 severity intheelderly. | |
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Cell Research (2021)31:415–432;https://doi.org/10.1038/s41422-020-00412-6 | |
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