2025
CYP1B1-AS1 regulates CYP1B1 to promote Coxiella burnetii pathogenesis by inhibiting ROS and host cell death
Arunima A, Niyakan S, Butler S, Clark S, Pinson A, Kwak D, Case E, Qian X, de Figueiredo P, van Schaik E, Samuel J. CYP1B1-AS1 regulates CYP1B1 to promote Coxiella burnetii pathogenesis by inhibiting ROS and host cell death. Nature Communications 2025, 16: 7493. PMID: 40796858, PMCID: PMC12344041, DOI: 10.1038/s41467-025-62762-2.Peer-Reviewed Original ResearchConceptsMitochondrial homeostasisTranscriptome analysisRegulation of mitochondrial homeostasisHost cell deathAnti-pathogen responsesCausative agentNuclear translocation assayAgent of Q feverBidirectional promoterNon-coding RNAsCausative agent of Q feverCo-regulationTranslocation assayCore setLncRNA researchLong non-coding RNAsCell deathPromoter assayMitochondrial dysfunctionIntracellular environmentSpatiotemporal mannerHost macrophagesRegulation of inflammationTHP-1 macrophagesAhR signalingMetabolic switches in cell death regulation
Galluzzi L. Metabolic switches in cell death regulation. Cell Metabolism 2025, 37: 1252-1254. PMID: 40466623, DOI: 10.1016/j.cmet.2025.04.017.Peer-Reviewed Original ResearchHarmonizing TUNEL with multiplexed iterative immunofluorescence enriches spatial contextualization of cell death
Sherman M, McMahon-Skates T, Gaston L, Katzen S, Majzoub J, Goessling W. Harmonizing TUNEL with multiplexed iterative immunofluorescence enriches spatial contextualization of cell death. Cell Reports Methods 2025, 5: 101047. PMID: 40359937, PMCID: PMC12146639, DOI: 10.1016/j.crmeth.2025.101047.Peer-Reviewed Original ResearchConceptsTerminal deoxynucleotidyl transferase dUTP nick end labelingCell deathTerminal deoxynucleotidyl transferase dUTP nick end labeling signalsProteinase K treatmentSpatial proteomicsProtein antigensProteomic methodsDUTP nick end labelingDeoxynucleotidyl transferase dUTP nick end labelingTransferase dUTP nick end labelingNick end labelingComplex tissuesK treatmentAntigen retrieval methodProteinHepatocyte necrosisAntigenProteomicsImmunofluorescenceCyclic immunofluorescence
2024
Pushing the Frontiers of Cancer Research: Highlights from the Frontiers in Cancer Science Conference 2023.
Lee Y, Chen L, Chew V, Chow E, Deng L, Hunziker W, Lee A, Leong G, Ngeow J, Pervaiz S, Sabapathy K, Skanderup A, Sundar R, Tay Y, Virshup D, Wong S, Tergaonkar V, Tam W. Pushing the Frontiers of Cancer Research: Highlights from the Frontiers in Cancer Science Conference 2023. Cancer Research 2024, 84: 1195-1198. PMID: 38616656, DOI: 10.1158/0008-5472.can-24-0721.Commentaries, Editorials and LettersSiponimod Attenuates Neuronal Cell Death Triggered by Neuroinflammation via NFκB and Mitochondrial Pathways
Gurrea-Rubio M, Wang Q, Mills E, Wu Q, Pitt D, Tsou P, Fox D, Mao-Draayer Y. Siponimod Attenuates Neuronal Cell Death Triggered by Neuroinflammation via NFκB and Mitochondrial Pathways. International Journal Of Molecular Sciences 2024, 25: 2454. PMID: 38473703, PMCID: PMC10931690, DOI: 10.3390/ijms25052454.Peer-Reviewed Original ResearchConceptsSecondary progressive MSRelapsing-remitting MSCentral nervous systemMultiple sclerosisProgressive MSModulator of sphingosine-1-phosphateCytokine tumor necrosis factor-alphaEffects of siponimodTumor necrosis factor-alphaHeterogeneous clinical courseBouts of inflammationNeuroprotective effectsPreclinical animal modelsAutoimmune demyelinating diseaseNecrosis factor-alphaMitochondrial oxidative phosphorylationHuman induced pluripotent stem cell (iPSC)-derived neuronsSphingosine-1-PhosphateCytokine Signaling PathwaysClinical courseLive cell analysisProgressive diseaseOral treatmentMitochondrial pathwayFactor-alphaIntracellular calcium links milk stasis to lysosome-dependent cell death during early mammary gland involution
Jeong J, Lee J, Talaia G, Kim W, Song J, Hong J, Yoo K, Gonzalez D, Athonvarangkul D, Shin J, Dann P, Haberman A, Kim L, Ferguson S, Choi J, Wysolmerski J. Intracellular calcium links milk stasis to lysosome-dependent cell death during early mammary gland involution. Cellular And Molecular Life Sciences 2024, 81: 29. PMID: 38212474, PMCID: PMC10784359, DOI: 10.1007/s00018-023-05044-8.Peer-Reviewed Original Research
2023
Profilin1 is required to prevent mitotic catastrophe in murine and human glomerular diseases
Tian X, Pedigo C, Li K, Ma X, Bunda P, Pell J, Lek A, Gu J, Zhang Y, Rangel P, Li W, Schwartze E, Nagata S, Lerner G, Perincheri S, Priyadarshini A, Zhao H, Lek M, Menon M, Fu R, Ishibe S. Profilin1 is required to prevent mitotic catastrophe in murine and human glomerular diseases. Journal Of Clinical Investigation 2023, 133: e171237. PMID: 37847555, PMCID: PMC10721156, DOI: 10.1172/jci171237.Peer-Reviewed Original ResearchConceptsProteinuric kidney diseaseKidney diseasePodocyte lossHuman glomerular diseasesMitotic catastrophePodocyte cell cycleSevere proteinuriaCell cycle reentryKidney failureGlomerular diseaseCell cycleKidney tissueG1/S checkpointUnsuccessful repairCyclin D1Glomerular integrityIrregular nucleiTissue-specific lossMouse podocytesPodocytesAltered expressionDiseaseCyclin B1Ribosome affinity purificationMultinucleated cellsPANoptosis in cancer, the triangle of cell death
Cai H, Lv M, Wang T. PANoptosis in cancer, the triangle of cell death. Cancer Medicine 2023, 12: 22206-22223. PMID: 38069556, PMCID: PMC10757109, DOI: 10.1002/cam4.6803.Peer-Reviewed Original ResearchApoptotic cell death in disease—Current understanding of the NCCD 2023
Vitale I, Pietrocola F, Guilbaud E, Aaronson S, Abrams J, Adam D, Agostini M, Agostinis P, Alnemri E, Altucci L, Amelio I, Andrews D, Aqeilan R, Arama E, Baehrecke E, Balachandran S, Bano D, Barlev N, Bartek J, Bazan N, Becker C, Bernassola F, Bertrand M, Bianchi M, Blagosklonny M, Blander J, Blandino G, Blomgren K, Borner C, Bortner C, Bove P, Boya P, Brenner C, Broz P, Brunner T, Damgaard R, Calin G, Campanella M, Candi E, Carbone M, Carmona-Gutierrez D, Cecconi F, Chan F, Chen G, Chen Q, Chen Y, Cheng E, Chipuk J, Cidlowski J, Ciechanover A, Ciliberto G, Conrad M, Cubillos-Ruiz J, Czabotar P, D’Angiolella V, Daugaard M, Dawson T, Dawson V, De Maria R, De Strooper B, Debatin K, Deberardinis R, Degterev A, Del Sal G, Deshmukh M, Di Virgilio F, Diederich M, Dixon S, Dynlacht B, El-Deiry W, Elrod J, Engeland K, Fimia G, Galassi C, Ganini C, Garcia-Saez A, Garg A, Garrido C, Gavathiotis E, Gerlic M, Ghosh S, Green D, Greene L, Gronemeyer H, Häcker G, Hajnóczky G, Hardwick J, Haupt Y, He S, Heery D, Hengartner M, Hetz C, Hildeman D, Ichijo H, Inoue S, Jäättelä M, Janic A, Joseph B, Jost P, Kanneganti T, Karin M, Kashkar H, Kaufmann T, Kelly G, Kepp O, Kimchi A, Kitsis R, Klionsky D, Kluck R, Krysko D, Kulms D, Kumar S, Lavandero S, Lavrik I, Lemasters J, Liccardi G, Linkermann A, Lipton S, Lockshin R, López-Otín C, Luedde T, MacFarlane M, Madeo F, Malorni W, Manic G, Mantovani R, Marchi S, Marine J, Martin S, Martinou J, Mastroberardino P, Medema J, Mehlen P, Meier P, Melino G, Melino S, Miao E, Moll U, Muñoz-Pinedo C, Murphy D, Niklison-Chirou M, Novelli F, Núñez G, Oberst A, Ofengeim D, Opferman J, Oren M, Pagano M, Panaretakis T, Pasparakis M, Penninger J, Pentimalli F, Pereira D, Pervaiz S, Peter M, Pinton P, Porta G, Prehn J, Puthalakath H, Rabinovich G, Rajalingam K, Ravichandran K, Rehm M, Ricci J, Rizzuto R, Robinson N, Rodrigues C, Rotblat B, Rothlin C, Rubinsztein D, Rudel T, Rufini A, Ryan K, Sarosiek K, Sawa A, Sayan E, Schroder K, Scorrano L, Sesti F, Shao F, Shi Y, Sica G, Silke J, Simon H, Sistigu A, Stephanou A, Stockwell B, Strapazzon F, Strasser A, Sun L, Sun E, Sun Q, Szabadkai G, Tait S, Tang D, Tavernarakis N, Troy C, Turk B, Urbano N, Vandenabeele P, Vanden Berghe T, Vander Heiden M, Vanderluit J, Verkhratsky A, Villunger A, von Karstedt S, Voss A, Vousden K, Vucic D, Vuri D, Wagner E, Walczak H, Wallach D, Wang R, Wang Y, Weber A, Wood W, Yamazaki T, Yang H, Zakeri Z, Zawacka-Pankau J, Zhang L, Zhang H, Zhivotovsky B, Zhou W, Piacentini M, Kroemer G, Galluzzi L. Apoptotic cell death in disease—Current understanding of the NCCD 2023. Cell Death & Differentiation 2023, 30: 1097-1154. PMID: 37100955, PMCID: PMC10130819, DOI: 10.1038/s41418-023-01153-w.Peer-Reviewed Original ResearchConceptsRegulated cell deathCell deathAdult tissue homeostasisMultiple human disordersApoptotic cell deathOrganismal developmentOrganismal homeostasisMolecular machineryContext of diseaseApoptotic apparatusMammalian systemsCaspase familyTissue homeostasisGenetic strategiesHuman disordersNomenclature CommitteeApoptosisHomeostasisMachineryOncogenesisProteaseCell lossActivationFamilyDeathNLRX1 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 speciesPUFAs dictate the balance of power in ferroptosis
Xin S, Schick J. PUFAs dictate the balance of power in ferroptosis. Cell Calcium 2023, 110: 102703. PMID: 36773492, DOI: 10.1016/j.ceca.2023.102703.Peer-Reviewed Original ResearchConceptsLethal lipid peroxidationIron-dependent formFerroptosis susceptibilityLipid remodelingFerroptosis sensitivityFatty acidsFerroptosis resistanceLipid transportersTumor suppressionMembrane lipidsPhospholipid transporterCell deathFerroptosis inductionBiochemical processesFerroptosisLipid metabolismReceptor alphaLipid componentsTransportersPeroxisome proliferatorLipid peroxidationCholesterol estersRegulatorAcidPPARA
2022
Cellular recovery after prolonged warm ischaemia of the whole body
Andrijevic D, Vrselja Z, Lysyy T, Zhang S, Skarica M, Spajic A, Dellal D, Thorn SL, Duckrow RB, Ma S, Duy PQ, Isiktas AU, Liang D, Li M, Kim SK, Daniele SG, Banu K, Perincheri S, Menon MC, Huttner A, Sheth KN, Gobeske KT, Tietjen GT, Zaveri HP, Latham SR, Sinusas AJ, Sestan N. Cellular recovery after prolonged warm ischaemia of the whole body. Nature 2022, 608: 405-412. PMID: 35922506, PMCID: PMC9518831, DOI: 10.1038/s41586-022-05016-1.Peer-Reviewed Original ResearchConceptsSingle-nucleus transcriptomic analysesSpecific gene expression patternsCellular recoveryGene expression patternsCellular processesMammalian cellsTranscriptomic analysisLarge mammalsExpression patternsCellular repair processesCell deathComprehensive resourceUnderappreciated potentialPhysiological challengesTissue integrityRepair processSpecific changesPorcine brainMammalsOrgansMultiple organsCell death in development, maintenance, and diseases of the nervous system
Mercau ME, Patwa S, Bhat KPL, Ghosh S, Rothlin CV. Cell death in development, maintenance, and diseases of the nervous system. Seminars In Immunopathology 2022, 44: 725-738. PMID: 35508671, DOI: 10.1007/s00281-022-00938-4.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsConceptsCell deathTissue-level responsesNervous system homeostasisNervous systemCentral nervous system tumorsMolecular modalitiesAcute brain injuryNervous system tumorsChronic neurodegenerative diseasesSystem homeostasisDead cellsNew therapeutic strategiesNeurodegenerative diseasesMechanisms of disposalGlial cellsNovel understandingAdult neurogenesisSystem tumorsBrain injuryPathological responseDisease statesTherapeutic strategiesCellsRecent studiesDeathMitochondrial ATP synthase c-subunit leak channel triggers cell death upon loss of its F1 subcomplex
Mnatsakanyan N, Park HA, Wu J, He X, Llaguno MC, Latta M, Miranda P, Murtishi B, Graham M, Weber J, Levy RJ, Pavlov EV, Jonas EA. Mitochondrial ATP synthase c-subunit leak channel triggers cell death upon loss of its F1 subcomplex. Cell Death & Differentiation 2022, 29: 1874-1887. PMID: 35322203, PMCID: PMC9433415, DOI: 10.1038/s41418-022-00972-7.Peer-Reviewed Original ResearchConceptsMitochondrial permeability transitionATP synthase c-subunitCell deathMitochondrial ATP synthaseChannel activityCellular energy productionLeak channelsVoltage-gated ion channelsF1 subcomplexATP synthaseC subunitInner membraneProkaryotic hostsCell stressPermeability transitionIon channelsGating mechanismOsmotic changesLarge conductanceC-ringChannels triggersNeuronal deathF1SubcomplexOsmotic gradientGhost mitochondria drive metastasis through adaptive GCN2/Akt therapeutic vulnerability
Ghosh JC, Perego M, Agarwal E, Bertolini I, Wang Y, Goldman AR, Tang HY, Kossenkov AV, Landis CJ, Languino LR, Plow EF, Morotti A, Ottobrini L, Locatelli M, Speicher DW, Caino MC, Cassel J, Salvino JM, Robert ME, Vaira V, Altieri DC. Ghost mitochondria drive metastasis through adaptive GCN2/Akt therapeutic vulnerability. Proceedings Of The National Academy Of Sciences Of The United States Of America 2022, 119: e2115624119. PMID: 35177476, PMCID: PMC8872753, DOI: 10.1073/pnas.2115624119.Peer-Reviewed Original ResearchMeSH KeywordsCell DeathCell Line, TumorCell MovementCell ProliferationEpithelial-Mesenchymal TransitionHumansMitochondriaMitochondrial DynamicsMitochondrial ProteinsMuscle ProteinsNeoplasm InvasivenessNeoplasm MetastasisNeoplasmsNeoplastic ProcessesProtein Serine-Threonine KinasesProto-Oncogene Proteins c-aktReactive Oxygen SpeciesSignal TransductionConceptsEpithelial-mesenchymal transitionGene expression programsTherapeutic vulnerabilitiesTumor cell movementCytokine/chemokine signalingExpression programsTherapeutic targetCell movementMitochondrial dynamicsEssential scaffoldMitochondrial structureSurvival signalingMitochondrial integrityCancer metabolismStress responseActionable therapeutic targetsCell deathChemokine signalingMitochondriaSmall-molecule drug screensCell proliferationOxidative damageInnate immunityMetastatic disseminationHuman tumorsGenome-wide identification of the genetic basis of amyotrophic lateral sclerosis
Zhang S, Cooper-Knock J, Weimer A, Shi M, Moll T, Marshall J, Harvey C, Nezhad H, Franklin J, dos Santos Souza C, Ning K, Wang C, Li J, Dilliott A, Farhan S, Elhaik E, Pasniceanu I, Livesey M, Eitan C, Hornstein E, Kenna K, Consortium P, Blair I, Wray N, Kiernan M, Neto M, Chio A, Cauchi R, Robberecht W, van Damme P, Corcia P, Couratier P, Hardiman O, McLaughin R, Gotkine M, Drory V, Ticozzi N, Silani V, Veldink J, van den Berg L, de Carvalho M, Pardina J, Povedano M, Andersen P, Weber M, Başak N, Al-Chalabi A, Shaw C, Shaw P, Morrison K, Landers J, Glass J, Veldink J, Ferraiuolo L, Shaw P, Snyder M. Genome-wide identification of the genetic basis of amyotrophic lateral sclerosis. Neuron 2022, 110: 992-1008.e11. PMID: 35045337, PMCID: PMC9017397, DOI: 10.1016/j.neuron.2021.12.019.Peer-Reviewed Original ResearchConceptsGenome-wide association studiesGenetic basisGenome-wide association study summary statisticsEpigenetic profilesAmyotrophic lateral sclerosisAmyotrophic lateral sclerosis genesComplex diseasesGenome-wide identificationRare variant analysisALS-associated genesTDP-43 mislocalizationGene discoveryFunctional genomicsAssociation studiesExtensive conservationCandidate genesGenetic convergencePathology of amyotrophic lateral sclerosisDiseased motor neuronsPatient mutationsVariant analysisLateral sclerosisTDP-43GenesKANK1
2021
Interdependent Regulation of Polycystin Expression Influences Starvation-Induced Autophagy and Cell Death
Decuypere JP, Van Giel D, Janssens P, Dong K, Somlo S, Cai Y, Mekahli D, Vennekens R. Interdependent Regulation of Polycystin Expression Influences Starvation-Induced Autophagy and Cell Death. International Journal Of Molecular Sciences 2021, 22: 13511. PMID: 34948309, PMCID: PMC8706473, DOI: 10.3390/ijms222413511.Peer-Reviewed Original ResearchConceptsProximal tubular epithelial cellsAutosomal dominant polycystic kidney diseaseEarly-stage ADPKD patientsCell deathPC2 expressionDominant polycystic kidney diseaseTubular epithelial cellsRenal cell survivalPolycystin-1Polycystic kidney diseaseCell survivalPolycystin-2Basal autophagyAutophagic cell survivalCell death resistanceADPKD progressionKidney diseaseADPKD patientsLess cell deathPC1 levelsChronic starvationHealthy individualsDuct cellsEpithelial cellsDeathDifferential pre-malignant programs and microenvironment chart distinct paths to malignancy in human colorectal polyps
Chen B, Scurrah CR, McKinley ET, Simmons AJ, Ramirez-Solano MA, Zhu X, Markham NO, Heiser CN, Vega PN, Rolong A, Kim H, Sheng Q, Drewes JL, Zhou Y, Southard-Smith AN, Xu Y, Ro J, Jones AL, Revetta F, Berry LD, Niitsu H, Islam M, Pelka K, Hofree M, Chen JH, Sarkizova S, Ng K, Giannakis M, Boland GM, Aguirre AJ, Anderson AC, Rozenblatt-Rosen O, Regev A, Hacohen N, Kawasaki K, Sato T, Goettel JA, Grady WM, Zheng W, Washington MK, Cai Q, Sears CL, Goldenring JR, Franklin JL, Su T, Huh WJ, Vandekar S, Roland JT, Liu Q, Coffey RJ, Shrubsole MJ, Lau KS. Differential pre-malignant programs and microenvironment chart distinct paths to malignancy in human colorectal polyps. Cell 2021, 184: 6262-6280.e26. PMID: 34910928, PMCID: PMC8941949, DOI: 10.1016/j.cell.2021.11.031.Peer-Reviewed Original ResearchMeSH KeywordsAdaptive ImmunityAdenomaAdultAgedAnimalsCarcinogenesisCell DeathCell DifferentiationColonic PolypsColorectal NeoplasmsDisease ProgressionFemaleGene Expression Regulation, NeoplasticGene Regulatory NetworksGenetic HeterogeneityHumansMaleMiceMiddle AgedMutationNeoplastic Stem CellsReproducibility of ResultsRNA-SeqSingle-Cell AnalysisTumor MicroenvironmentConceptsHuman colorectal polypsColorectal cancerColorectal polypsPrevention of CRCMicrosatellite-unstable colorectal cancersUnstable colorectal cancersGastric metaplasiaImmune microenvironmentTumor cell differentiation statusImmune cellsPrecision surveillancePrecursor polypsSerrated polypsConventional adenomasStem cell propertiesMalignant progressionImmunogenic potentialPolypsTumor cellsTherapeutic insightsCell differentiation statusCellular originMetaplasiaAdenomasMolecular heterogeneityExogenous inter-α inhibitor proteins prevent cell death and improve ischemic stroke outcomes in mice
McCullough LD, Roy-O’Reilly M, Lai YJ, Patrizz A, Xu Y, Lee J, Holmes A, Kraushaar DC, Chauhan A, Sansing LH, Stonestreet BS, Zhu L, Kofler J, Lim YP, Venna VR. Exogenous inter-α inhibitor proteins prevent cell death and improve ischemic stroke outcomes in mice. Journal Of Clinical Investigation 2021, 131: e144898. PMID: 34580244, PMCID: PMC8409590, DOI: 10.1172/jci144898.Peer-Reviewed Original ResearchConceptsInter-α inhibitor proteinsIschemic strokeStroke outcomeStroke modelComplement activationBeneficial effectsMultiple stroke modelsNeutralization of histonesPost-stroke administrationIschemic stroke outcomeExperimental ischemic strokeIschemic stroke patientsExperimental stroke modelsModel of sepsisPotential therapeutic candidateExcess complement activationIaIp levelsStroke onsetStroke patientsProinflammatory cytokinesAged miceExtracellular histonesClinical relevanceTherapeutic candidateTherapeutic efficacyEndocytosis and the Participation of Glycosaminoglycans Are Important to the Mechanism of Cell Death Induced by β‑Hairpin Antimicrobial Peptides
Buri M, Sperandio L, de Souza K, Antunes F, Rezende M, Melo C, Pinhal M, Barros C, Fernig D, Yates E, Ide J, Smaili S, Riske K, Nader H, dos Santos Tersariol I, Lima M, Judice W, Miranda A, Paredes-Gamero E. Endocytosis and the Participation of Glycosaminoglycans Are Important to the Mechanism of Cell Death Induced by β‑Hairpin Antimicrobial Peptides. ACS Applied Bio Materials 2021, 4: 6488-6501. PMID: 35006908, DOI: 10.1021/acsabm.1c00390.Peer-Reviewed Original ResearchConceptsCell deathAntimicrobial peptidesSecondary structure homologyControl cell deathΒ-hairpin antimicrobial peptidesCommon mechanismCytotoxicity of AMPsStructure homologyMembrane permeabilizationGene expressionMitochondrial potentialCytotoxic modeEndocytosisCell membraneCell tumor modelΒ-hairpin peptidesAMP stimulationPeptidesDynaminHomologyPermeabilizationGlycosaminoglycansMechanismProteinCytotoxicity
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