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 ResearchConceptsCellular 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
2020
Recent Advances in Molecular Basis of Lung Aging and Its Associated Diseases
Kang M. Recent Advances in Molecular Basis of Lung Aging and Its Associated Diseases. Tuberculosis And Respiratory Diseases 2020, 83: 107-115. PMID: 32185913, PMCID: PMC7105435, DOI: 10.4046/trd.2020.0003.Peer-Reviewed Original ResearchAging-related lung disordersLung disordersChronic obstructive pulmonary diseaseMajor unmet medical needObstructive pulmonary diseaseChronic lung disordersIdiopathic pulmonary fibrosisMolecular basisMolecular featuresBiological functionsUnmet medical needMolecular mechanismsCrucial risk factorMolecular understandingMolecular biologyBiologyPulmonary diseaseLung agingPulmonary fibrosisRisk factorsAdvanced agePulmonary medicineAssociated diseaseMedical needProgressive decline