Nucleotide‐binding domain and leucine‐rich‐repeat‐containing protein X1 deficiency induces nicotinamide adenine dinucleotide decline, mechanistic target of rapamycin activation, and cellular senescence and accelerates aging lung‐like changes
Shin HJ, Kim S, Park H, Shin M, Kang I, Kang M. Nucleotide‐binding domain and leucine‐rich‐repeat‐containing protein X1 deficiency induces nicotinamide adenine dinucleotide decline, mechanistic target of rapamycin activation, and cellular senescence and accelerates aging lung‐like changes. Aging Cell 2021, 20: e13410. PMID: 34087956, PMCID: PMC8282248, DOI: 10.1111/acel.13410.Peer-Reviewed Original ResearchMeSH KeywordsAgingAnimalsCellular SenescenceHumansLungMiceMitochondrial ProteinsNLR ProteinsSirolimusConceptsCellular senescenceActivation of mTORNucleotide-binding domainCellular senescence responseReplicative cellular senescenceNLR family membersOrganismal agingCellular physiologyMitochondrial moleculesSenescence responseCellular locationProtein X1Crucial regulatorMechanistic targetMitochondrial functionMolecular hallmarksNLRX1 functionRapamycin (mTOR) activationMitochondrial dysfunctionSenescenceMTORPharmacological inhibitionNLRX1BiologyAging LungMacrophage-preferable delivery of the leucine-rich repeat domain of NLRX1 ameliorates lethal sepsis by regulating NF-κB and inflammasome signaling activation
Koo JH, Kim SH, Jeon SH, Kang MJ, Choi JM. Macrophage-preferable delivery of the leucine-rich repeat domain of NLRX1 ameliorates lethal sepsis by regulating NF-κB and inflammasome signaling activation. Biomaterials 2021, 274: 120845. PMID: 33971559, DOI: 10.1016/j.biomaterials.2021.120845.Peer-Reviewed Original ResearchMeSH KeywordsHumansInflammasomesLeucineLipopolysaccharidesMacrophagesMitochondrial ProteinsNF-kappa BSepsisConceptsSystemic inflammationSepsis modelNF-κBAcute systemic inflammatory diseaseSymptoms of sepsisSystemic inflammatory diseaseAnti-TNFα antibodyIL-6 productionIL-1β productionEffective therapeutic agentCaspase-1 activationOrgan dysfunctionLethal sepsisTreatment optionsInflammatory diseasesP65 phosphorylationSepsisIκB degradationBacterial infectionsPeritoneal macrophagesTherapeutic agentsMacrophagesInflammationInflammasomeLPS