2025
Adding insult to injury: the spectrum of tubulointerstitial responses in acute kidney injury
Baker M, Cantley L. Adding insult to injury: the spectrum of tubulointerstitial responses in acute kidney injury. Journal Of Clinical Investigation 2025, 135: e188358. PMID: 40091836, PMCID: PMC11910233, DOI: 10.1172/jci188358.Peer-Reviewed Original ResearchConceptsAcute kidney injuryTubular epithelial cellsKidney injuryTubular cellsCases of acute kidney injuryImmune-mediated processPersistence of inflammationBiphasic immune responseChronic kidney diseaseCell deathTubular cell injuryLymphocyte subsetsTubular repairCell cycle arrestOutflow obstructionTEC differentiationPreclinical findingsLymphocytic infiltrationProinflammatory macrophagesKidney diseaseModulate inflammationImmune responseActivated macrophagesMetabolic reprogrammingTubular castsNorovirus co-opts NINJ1 for selective protein secretion
Song J, Zhang L, Moon S, Fang A, Wang G, Gheshm N, Loeb S, Cao P, Wallace J, Alfajaro M, Strine M, Beatty W, Jamieson A, Orchard R, Robinson B, Nice T, Wilen C, Orvedahl A, Reese T, Lee S. Norovirus co-opts NINJ1 for selective protein secretion. Science Advances 2025, 11: eadu7985. PMID: 40020060, PMCID: PMC11870086, DOI: 10.1126/sciadv.adu7985.Peer-Reviewed Original ResearchConceptsPlasma membrane ruptureDamage-associated molecular patternsNS1 secretionNinjurin-1Programmed cell deathAmino acid residuesViral replication sitesViral protein NS1CRISPR screensIntracellular viral proteinsMutagenesis studiesMembrane ruptureProtein NS1Unconventional pathwayCaspase-3Protein secretionViral proteinsReplication sitesCell deathMolecular patternsGenetic ablationNS1Pharmaceutical inhibitionDAMP releaseProteinS-Nitrosylation of CRTC1 in Alzheimer’s disease impairs CREB-dependent gene expression induced by neuronal activity
Zhang X, Vlkolinsky R, Wu C, Dolatabadi N, Scott H, Prikhodko O, Zhang A, Blanco M, Lang N, Piña-Crespo J, Nakamura T, Roberto M, Lipton S. S-Nitrosylation of CRTC1 in Alzheimer’s disease impairs CREB-dependent gene expression induced by neuronal activity. Proceedings Of The National Academy Of Sciences Of The United States Of America 2025, 122: e2418179122. PMID: 40014571, PMCID: PMC11892585, DOI: 10.1073/pnas.2418179122.Peer-Reviewed Original ResearchConceptsActivity-dependent gene expressionGene expressionAlzheimer's diseaseCREB-dependent gene expressionS-nitrosylationNitric oxide (NO)-related speciesTargets of S-nitrosylationNeuronal activity-dependent gene expressionPathogenesis of ADDecreased neurite lengthIncreased neuronal cell deathNeuronal cell deathSynaptic plasticityTranscriptional pathwaysCell deathCRISPR/Cas9 techniqueTranscription coactivator 1AD modelLong-term memory formationIncreased S-nitrosylationLong-term potentiationTherapeutic targetExpressionNeurite lengthCerebrocortical neurons
2024
Immunogenicity of cell death and cancer immunotherapy with immune checkpoint inhibitors
Catanzaro E, Beltrán-Visiedo M, Galluzzi L, Krysko D. Immunogenicity of cell death and cancer immunotherapy with immune checkpoint inhibitors. Cellular & Molecular Immunology 2024, 22: 24-39. PMID: 39653769, PMCID: PMC11685666, DOI: 10.1038/s41423-024-01245-8.Peer-Reviewed Original ResearchImmune checkpoint inhibitorsImmunogenic cell deathImmunogenic cell death inducerCheckpoint inhibitorsRefractory to immune checkpoint inhibitorsImmunogenicity of cell deathFraction of patientsCombinatorial treatment strategiesAdaptive immune responsesCell deathCombinatorial partnersCancer immunotherapyCombinatorial regimensClinical findingsClinical managementTreatment strategiesClinical activityImmune responseImmunotherapyPatientsCancerOncology settingInhibitorsDeathInducerDevelopment of a small molecule-based two-photon photosensitizer for targeting cancer cells
Lee D, Cao Y, Juvekar V, Sauraj, Noh C, Shin S, Liu Z, Kim H. Development of a small molecule-based two-photon photosensitizer for targeting cancer cells. Journal Of Materials Chemistry B 2024, 12: 12232-12238. PMID: 39469993, DOI: 10.1039/d4tb01706d.Peer-Reviewed Original ResearchConceptsTarget cancer cellsReactive oxygen speciesPhotodynamic therapyCancer cellsDiverse cell linesInduced ROS productionColon cancer tissuesTwo-photon (TPCell deathLow dark toxicityCancer modelsTwo-photon photosensitizerROS productionCancer selectivityInduce cell damageThree-dimensional spheroidsCell linesTP excitationImaging-guided photodynamic therapyCancer tissuesOxygen speciesTP-PDTFerroptosis in Osteoarthritis: Towards Novel Therapeutic Strategy
Zhang Y, Li J, Liu J, Gao Y, Li K, Zhao X, Liu Y, Wang D, Hu X, Wang Z. Ferroptosis in Osteoarthritis: Towards Novel Therapeutic Strategy. Cell Proliferation 2024, 58: e13779. PMID: 39624950, PMCID: PMC11882765, DOI: 10.1111/cpr.13779.Peer-Reviewed Original ResearchArticular cartilageTherapeutic strategiesChondrocyte viabilityCell deathMechanical stressNovel therapeutic strategiesOA cartilagePotential therapeutic strategyIron-dependent formPersistent painRegulated cell deathAutophagic cell deathIron overloadPathogenetic mechanismsExtracellular matrix integrityInflammatory responseIdentification of High-Efficiency β-Catenin Protein Degradation As Critical Vulnerability in B-Cell Malignancies
Cosgun K, Robinson M, Agadzhanian N, Cheng Z, Oulghazi S, Berning P, Fonseca-Arce D, Kume K, Fontaine J, Chan L, Lee J, Yu F, Qian Z, Song J, Chan W, Chen J, Taketo M, Schjerven H, Müschen M. Identification of High-Efficiency β-Catenin Protein Degradation As Critical Vulnerability in B-Cell Malignancies. Blood 2024, 144: 4125-4125. DOI: 10.1182/blood-2024-208125.Peer-Reviewed Original ResearchProtein degradation pathwaysB-ALL cellsProtein degradationRepression of MYCTranscriptional activity of MYCCell deathAcute cell deathLoss of colony formationChIP-seq analysisActive enhancer marksB-cell malignanciesSuper-enhancer regionsActivation of MYCIkaros transcription factorB-lymphoid cellsCell linesB cell identityDefective protein degradationB-cateninNon-lymphoid cell linesDegradation pathwayMantle cell lymphomaProtein levelsB-ALLChIP-seqTargeting β-Catenin Protein Degradation in Refractory B-Cell Malignancies
Cosgun K, Robinson M, Agadzhanian N, Berning P, Fonseca-Arce D, Leveille E, Kothari S, Davids M, Jellusova J, Müschen M. Targeting β-Catenin Protein Degradation in Refractory B-Cell Malignancies. Blood 2024, 144: 1412. DOI: 10.1182/blood-2024-208598.Peer-Reviewed Original ResearchProtein degradationRepression of MYCTranscriptional repression of MYCTranscriptional repressionPromote survivalProteasome inhibitorsProtein degradation pathwaysCell typesN-terminal residuesInduce cell deathRefractory B-cell malignanciesB-cateninB-cell malignanciesRNAi screenInteractome studiesB cell selectionRepressive complexesGene dependenciesProteasomal degradationB cellsChemogenomic screensProteasome inhibitor bortezomibActivated mycDeletion of Ctnnb1Cell deathMetabolic Determinants of Ferroptosis in B-Cell Lymphoma
Leveille E, Bramson E, Robinson M, Bertomeu T, Chatr-Aryamontri A, Kothari S, Müschen M. Metabolic Determinants of Ferroptosis in B-Cell Lymphoma. Blood 2024, 144: 976-976. DOI: 10.1182/blood-2024-209077.Peer-Reviewed Original ResearchB-cell lymphomaB-cell malignanciesB cellsSensitivity to ferroptosisLipid membrane remodelingFerroptosis inducersMyeloid leukemiaSolid tumorsMembrane remodelingCRISPR screensGene dependenciesAssociated with significantly worse survivalTreatment of B-cell lymphomaB-cell lymphoma modelElimination of B cellsPUFA metabolismCysteine-glutamate antiporterCell deathMature splenic B cellsTherapy-resistant tumorsNon-apoptotic form of cell deathAnalysis of clinical dataDominant-negative p53Vulnerability to ferroptosisWhole-genome CRISPR screenPARG inhibition induces nuclear aggregation of PARylated PARP1
Paradkar S, Purcell J, Cui A, Friedman S, Noronha K, Murray M, Sundaram R, Bindra R, Jensen R. PARG inhibition induces nuclear aggregation of PARylated PARP1. Structure 2024, 32: 2083-2093.e5. PMID: 39406247, DOI: 10.1016/j.str.2024.09.006.Peer-Reviewed Original ResearchFlaviviruses manipulate mitochondrial processes to evade the innate immune response
Boytz R, Keita K, Pawlak J, Laurent-Rolle M. Flaviviruses manipulate mitochondrial processes to evade the innate immune response. Npj Viruses 2024, 2: 47. PMID: 39371935, PMCID: PMC11452341, DOI: 10.1038/s44298-024-00057-x.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsMitochondrial processesAntiviral signaling proteinProgrammed cell deathRegulate various aspectsInnate immune response to viral infectionEukaryotic organellesResponse to viral infectionMitochondrial biologyInnate immune responseMitochondrial morphologyCellular processesSignaling proteinsCell deathImmune response to viral infectionInnate immunityMitochondriaCalcium homeostasisFlavivirusesViral infectionImmune responseOrganellesPathogensDynamic structureProteinHomeostasisCarrier-free multifunctional nanomedicine for enhanced hyperthermic intraperitoneal chemotherapy against abdominal pelvic tumors
Fang H, Zhang L, Wu Y, Chen L, Deng Z, Zheng Z, Wang Y, Yang Y, Chen Q. Carrier-free multifunctional nanomedicine for enhanced hyperthermic intraperitoneal chemotherapy against abdominal pelvic tumors. Chemical Engineering Journal 2024, 498: 155781. DOI: 10.1016/j.cej.2024.155781.Peer-Reviewed Original ResearchHyperthermic intraperitoneal chemotherapyImmunogenic cell deathDamage-associated molecular patternsPelvic tumorsIntraperitoneal chemotherapyGambogic acidAnti-tumor immune response in vivoInfiltration of cytotoxic T lymphocytesTriggering immunogenic cell deathRelease of damage-associated molecular patternsCancer cellsImmune responses in vivoCytotoxic T lymphocytesInduce apoptosis of cancer cellsApoptosis of cancer cellsResponses in vivoInhibitor of heat shock proteinCell deathHyperthermia-induced cell deathPenetration of nanoparticlesTumor extracellular matrixHeat shock proteinsOvarian cancerTumor microenvironmentT lymphocytesChitinase 3-like-1 Inhibits Innate Antitumor and Tissue Remodeling Immune Responses by Regulating CD47-SIRPα- and CD24-Siglec10-Mediated Phagocytosis.
Ma B, Kamle S, Sadanaga T, Lee C, Lee J, Yee D, Zhu Z, Silverman E, DeMeo D, Choi A, Lee C, Elias J. Chitinase 3-like-1 Inhibits Innate Antitumor and Tissue Remodeling Immune Responses by Regulating CD47-SIRPα- and CD24-Siglec10-Mediated Phagocytosis. The Journal Of Immunology 2024, 213: 1279-1291. PMID: 39291933, DOI: 10.4049/jimmunol.2400035.Peer-Reviewed Original ResearchImmune checkpoint moleculesChronic obstructive pulmonary diseaseInhibit adaptive immune responsesAdaptive immune responsesInnate immune responseImmune responseInhibition of innate immune responsesInhibits T cell costimulationGeneration of adaptive immune responsesMacrophage phagocytosisInhibit innate immune responsesChitinase 3-like 1T cell costimulationEpithelial cell deathObstructive pulmonary diseaseCheckpoint moleculesPoor prognosisLung injuryInhibit macrophagesPulmonary diseaseCHI3L1Inflammation pathwaysCancerSHP-2 phosphataseCell deathStem cells tightly regulate dead cell clearance to maintain tissue fitness
Stewart K, Abdusselamoglu M, Tierney M, Gola A, Hur Y, Gonzales K, Yuan S, Bonny A, Yang Y, Infarinato N, Cowley C, Levorse J, Pasolli H, Ghosh S, Rothlin C, Fuchs E. Stem cells tightly regulate dead cell clearance to maintain tissue fitness. Nature 2024, 633: 407-416. PMID: 39169186, PMCID: PMC11390485, DOI: 10.1038/s41586-024-07855-6.Peer-Reviewed Original ResearchStem cellsImmune-privileged nicheHair follicle stem cellsStem cell functionFollicle stem cellsTissue fitnessMesenchymal tissue cellsBillions of cellsDendritic cellsTissue stemProgenitor cellsPreserving tissue integrityDead cell clearanceClearance genesCell clearanceCell functionFunctional evidenceDying cellsHealthy counterpartsCell deathNon-motileTissue cellsHair cycleProfessional phagocytesApoptotic corpsesExploring a Novel Role of Glycerol Kinase 1 in Prostate Cancer PC-3 Cells
Park B, Kim S, Yu S, Kim K, Jeon H, Ahn S. Exploring a Novel Role of Glycerol Kinase 1 in Prostate Cancer PC-3 Cells. Biomolecules 2024, 14: 997. PMID: 39199385, PMCID: PMC11352368, DOI: 10.3390/biom14080997.Peer-Reviewed Original ResearchPC-3 cellsProstate cancer PC-3 cellsGK deficiencyCell deathProstate cancerAnti-cancer agentsKinase 1Apoptotic cell deathDNA microarray analysisHuman prostate cancer PC-3 cellsCancer cell deathModulating tumor microenvironmentProstate cancer cellsBiomarkers of cell deathX chromosomeReduced cell viabilityEpigenetic regulationExpression vectorInvestigated genesSynthesis of triglyceridesMicroarray analysisGenetic alterationsTumor microenvironmentNovel roleCancer cellsIntrinsic link between PGRN and Gba1 D409V mutation dosage in potentiating Gaucher disease
Lin Y, Zhao X, Liou B, Fannin V, Zhang W, Setchell K, Wang X, Pan D, Grabowski G, Liu C, Sun Y. Intrinsic link between PGRN and Gba1 D409V mutation dosage in potentiating Gaucher disease. Human Molecular Genetics 2024, 33: 1771-1788. PMID: 39101473, PMCID: PMC11458007, DOI: 10.1093/hmg/ddae113.Peer-Reviewed Original ResearchGaucher diseaseMutation dosageMouse modelDisease severityProgrammed cell deathRetinal gliosisBrain transcriptomic analysisGD pathogenesisPGRN deficiencyTissue fibrosisDisease progressionGrn-/- miceSevere phenotypeGlycosphingolipid accumulationTranscriptome analysisInflammatory responseGCase functionMiceCell deathShort life spanNeurobehavioral analysisDiseaseGCase activityNeurodegenerative diseasesPGRNMitochondria as therapeutic targets in assisted reproduction
Yildirim R, Seli E. Mitochondria as therapeutic targets in assisted reproduction. Human Reproduction 2024, 39: 2147-2159. PMID: 39066614, DOI: 10.1093/humrep/deae170.Peer-Reviewed Original ResearchMitochondrial replacement therapyClinical trialsAssisted reproductionImprove oocyte qualityTherapeutic targetAssisted reproductive outcomesImprove assisted reproductive outcomesMitochondrial quality control mechanismsDevelopmental competenceOocyte qualityReplacement therapyProgrammed cell deathQuality control mechanismsPharmacological agentsTargeting mitochondrial functionCalcium homeostasisReproductive outcomesInhibitor rapamycinMammalian targetMaternal spindle transferAntioxidant coenzyme Q10Mitochondrial populationEmbryo developmentCoenzyme Q10Cell deathMitochondrial network remodeling of the diabetic heart: implications to ischemia related cardiac dysfunction
Rudokas M, McKay M, Toksoy Z, Eisen J, Bögner M, Young L, Akar F. Mitochondrial network remodeling of the diabetic heart: implications to ischemia related cardiac dysfunction. Cardiovascular Diabetology 2024, 23: 261. PMID: 39026280, PMCID: PMC11264840, DOI: 10.1186/s12933-024-02357-1.Peer-Reviewed Original ResearchConceptsReactive oxygen speciesMitochondrial network remodelingDamaged mitochondrial DNAEfficiency of oxidative phosphorylationImpaired ATP productionMitochondrial ultrastructural alterationsCardiac functionDiabetic heartCellular energy metabolismProduction of reactive oxygen speciesMitochondrial DNAMitochondrial networkMitochondrial fissionExcessive production of reactive oxygen speciesOxidative phosphorylationATP productionResponse to ischemic insultGlobal cardiac functionCell deathOverall cardiac functionCardiac ischemic injuryResponse to injuryCardiac mitochondriaIrreversible cell deathMitochondriaMapping the influence of hydrocarbons mixture on molecular mechanisms, involved in breast and lung neoplasms: in silico toxicogenomic data-mining
Abu-Bakar A, Ismail M, Zulkifli M, Zaini N, Shukor N, Harun S, Inayat-Hussain S. Mapping the influence of hydrocarbons mixture on molecular mechanisms, involved in breast and lung neoplasms: in silico toxicogenomic data-mining. Genes And Environment 2024, 46: 15. PMID: 38982523, PMCID: PMC11232146, DOI: 10.1186/s41021-024-00310-y.Peer-Reviewed Original ResearchNon-apoptotic programmed cell deathSignaling pathwayMolecular mechanismsResponse to oxidative stressInterleukin-17 signaling pathwayMolecular pathwaysSurvival signaling pathwaysAdaptive response to oxidative stressOxidative stress responseBreast cancer invasionGenetic interactionsModulate IL-8Protein domainsCytoscape softwareAir pollutionCritical genesCell deathCo-expressionGenesRisk of breastStress responseToxicogenomic analysisToxicogenomics toolsDevelopment of breastInvestigated hydrocarbonsA review on polyamines as promising next-generation neuroprotective and anti-aging therapy
Arthur R, Jamwal S, Kumar P. A review on polyamines as promising next-generation neuroprotective and anti-aging therapy. European Journal Of Pharmacology 2024, 978: 176804. PMID: 38950837, DOI: 10.1016/j.ejphar.2024.176804.Peer-Reviewed Original ResearchCognitive dysfunctionNeurodegenerative disordersRegulation of gene expressionProgressive degeneration of neuronsProgrammed cell deathDegeneration of neuronsSymptomatic therapyPharmacological strategiesAnti-oxidative effectsAnti-aging therapyAverage ageProgressive degenerationNeuroprotective effectsLocomotor abnormalitiesIon channelsCell deathBiochemical activityGene expressionPopulation average ageTherapyMolecular mechanismsDisordersPolyamine supplementationDysfunctionAnti-aging effects
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