2023
NLRX1 knockdown attenuates pro-apoptotic signaling and cell death in pulmonary hyperoxic acute injury
Kim H, Kim M, Kim E, Leem J, Baek S, Lee Y, Kim K, Kang M, Song T, Sohn M. NLRX1 knockdown attenuates pro-apoptotic signaling and cell death in pulmonary hyperoxic acute injury. Scientific Reports 2023, 13: 3441. PMID: 36859435, PMCID: PMC9975446, DOI: 10.1038/s41598-023-28206-x.Peer-Reviewed Original ResearchMeSH KeywordsAcute Lung InjuryAnimalsApoptosisCell DeathHyperoxiaMiceMitochondrial ProteinsSignal TransductionConceptsHyperoxic acute lung injuryAcute lung injuryLung injuryWT miceAcute respiratory failurePro-inflammatory cytokinesCell deathRespiratory failureAcute injuryInflammatory cellsReduced mortalityRole of NLRX1Murine modelNLRX1 expressionPro-apoptotic signalingCell cytotoxicityHyperoxiaInjuryMiceProtein leakageHyperoxic conditionsNLRX1Apoptotic cell deathERK 1/2Reactive oxygen species
2021
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 Lung