2025
SIMVI disentangles intrinsic and spatial-induced cellular states in spatial omics data
Dong M, Su D, Kluger H, Fan R, Kluger Y. SIMVI disentangles intrinsic and spatial-induced cellular states in spatial omics data. Nature Communications 2025, 16: 2990. PMID: 40148341, PMCID: PMC11950362, DOI: 10.1038/s41467-025-58089-7.Peer-Reviewed Original ResearchConceptsOmics dataSpatial omics dataAnalysis of gene expressionSingle-cell resolutionDownstream analysisCellular statesSpatial interaction modelsGerminal center B cellsGene expressionCommunication machineryOmics technologiesIntercellular interactionsSpatial omics technologiesTumor microenvironmentB cellsSpatial dynamicsHuman tonsilsMacrophage stateSpatial effectsAn antibody–toxin conjugate targeting CD47 linked to the bacterial toxin listeriolysin O for cancer immunotherapy
Schrank B, Wang Y, Wu A, Tran N, Lee D, Edwards J, Huntoon K, Dong S, Ha J, Ma Y, Grippin A, Jeong S, Antony A, Chang M, Kang M, Gallup T, Koong A, Li J, Yun K, Kim B, Jiang W. An antibody–toxin conjugate targeting CD47 linked to the bacterial toxin listeriolysin O for cancer immunotherapy. Nature Cancer 2025, 6: 511-527. PMID: 40000910, DOI: 10.1038/s43018-025-00919-0.Peer-Reviewed Original ResearchConceptsAntibody-toxin conjugatesTumor cellsImmune recognition of tumor cellsEnhanced antigen cross-presentationRecognition of tumor cellsCancer cell phagocytosisTumor-derived antigensToxin listeriolysin OTumor-derived peptidesImproved animal survivalPromote immune recognitionCytosolic immune sensorsIntracellular bacterium Listeria monocytogenesTreatment in vivoTreating multiple cancersPhagocytosis checkpointsCheckpoint blockadeCancer immunotherapySignal CD47Listeriolysin OMetastatic breastMelanoma tumorsTherapeutic strategiesAnimal survivalCell phagocytosisCold and hot fibrosis define clinically distinct cardiac pathologies
Miyara S, Adler M, Umansky K, Häußler D, Bassat E, Divinsky Y, Elkahal J, Kain D, Lendengolts D, Flores R, Bueno-Levy H, Golani O, Shalit T, Gershovits M, Weizman E, Genzelinakh A, Kimchi D, Shakked A, Zhang L, Wang J, Baehr A, Petrover Z, Sarig R, Dorn T, Moretti A, Saez-Rodriguez J, Kupatt C, Tanaka E, Medzhitov R, Krüger A, Mayo A, Alon U, Tzahor E. Cold and hot fibrosis define clinically distinct cardiac pathologies. Cell Systems 2025, 16: 101198. PMID: 39970910, PMCID: PMC11922821, DOI: 10.1016/j.cels.2025.101198.Peer-Reviewed Original ResearchConceptsHeart failureMyocardial infarctionAutocrine growth factor loopsUnmet medical needCardiac fibrosisNeutralizing antibodiesReduced fibrosisTreatment strategiesMyofibroblast proliferationAcute MIFibrosis post-MICardiac pathologyFibrosisTherapeutic approachesPost-MIChronic injuryMyofibroblastsMedical needFactor loopsMulti-Scale Multi-Cell Computational Model of Inflammation-Mediated Aortic Remodeling in Hypertension
Estrada A, Humphrey J. Multi-Scale Multi-Cell Computational Model of Inflammation-Mediated Aortic Remodeling in Hypertension. Annals Of Biomedical Engineering 2025, 53: 1014-1023. PMID: 39904866, DOI: 10.1007/s10439-025-03685-3.Peer-Reviewed Original ResearchDeletion of sphingosine 1-phosphate receptor 1 in myeloid cells reduces hepatic inflammatory macrophages and attenuates MASH
Parthasarathy G, Venkatesan N, Sidhu G, Song M, Liao C, Barrow F, Mauer A, Sehrawat T, Nakao Y, Daniel P, Dasgupta D, Pavelko K, Revelo X, Malhi H. Deletion of sphingosine 1-phosphate receptor 1 in myeloid cells reduces hepatic inflammatory macrophages and attenuates MASH. Hepatology Communications 2025, 9: e0613. PMID: 39899672, DOI: 10.1097/hc9.0000000000000613.Peer-Reviewed Original ResearchConceptsMyeloid cellsMonocyte-derived macrophagesHigh-fatLiver injuryProinflammatory monocyte-derived macrophagesReceptor 1Cell-specific knockout miceMass cytometryT cell subsetsSphingosine 1-phosphate receptor 1Cardiometabolic risk factorsS1P receptor 1Accumulation of monocyte-derived macrophagesImmune cell typesWild-typeLiver inflammatory infiltrationGene ontology pathway analysisWild-type controlsDevelopment of steatohepatitisSphingosine 1-phosphateMitogen-activated protein kinase pathwayT cellsIntrahepatic macrophagesInflammatory infiltrateKnockout mice
2024
Malate initiates a proton-sensing pathway essential for pH regulation of inflammation
Chen Y, Shi R, Xiang Y, Fan L, Tang H, He G, Zhou M, Feng X, Tan J, Huang P, Ye X, Zhao K, Fu W, Li L, Bian X, Chen H, Wang F, Wang T, Zhang C, Zhou B, Chen W, Liang T, Lv J, Kang X, Shi Y, Kim E, Qin Y, Hettinghouse A, Wang K, Zhao X, Yang M, Tang Y, Piao H, Guo L, Liu C, Miao H, Tang K. Malate initiates a proton-sensing pathway essential for pH regulation of inflammation. Signal Transduction And Targeted Therapy 2024, 9: 367. PMID: 39737965, PMCID: PMC11683149, DOI: 10.1038/s41392-024-02076-9.Peer-Reviewed Original ResearchConceptsL-malateInflammatory responseCytosolic pHBind BiPTCA intermediatesSensing pathwaysRegulation of inflammatory responsesBiological informationAnti-inflammatory metabolitesAnti-inflammatory proteinPro-inflammatory macrophagesRegulation of inflammationSignaling modalitiesPhysiological adaptationsAnti-inflammatory effectsIRF2BP2BiPPH regulationCarboxylate metaboliteChemical languageIn vivoIn vitroMacrophagesPathwayPH reductionEzrin drives adaptation of monocytes to the inflamed lung microenvironment
Gudneppanavar R, Di Pietro C, H Öz H, Zhang P, Cheng E, Huang P, Tebaldi T, Biancon G, Halene S, Hoppe A, Kim C, Gonzalez A, Krause D, Egan M, Gupta N, Murray T, Bruscia E. Ezrin drives adaptation of monocytes to the inflamed lung microenvironment. Cell Death & Disease 2024, 15: 864. PMID: 39613751, PMCID: PMC11607083, DOI: 10.1038/s41419-024-07255-8.Peer-Reviewed Original ResearchConceptsActivation of focal adhesion kinaseExtracellular matrixActin-binding proteinsFocal adhesion kinaseLung extracellular matrixKnock-out mouse modelProtein kinase signalingCortical cytoskeletonLoss of ezrinKinase signalingPlasma membraneCell migrationSignaling pathwayEzrinResponse to lipopolysaccharideTissue-resident macrophagesMouse modelLipopolysaccharideCytoskeletonEzrin expressionLung microenvironmentKinaseMonocyte recruitmentProteinAktFeeding the wrath with myelin
Ghosh S, Rothlin C. Feeding the wrath with myelin. Trends In Immunology 2024, 45: 729-731. PMID: 39341708, PMCID: PMC11471388, DOI: 10.1016/j.it.2024.09.004.Peer-Reviewed Original ResearchMacrophage membrane-camouflaged biomimetic nanoparticles for rheumatoid arthritis treatment via modulating macrophage polarization
Zhou R, Xue S, Cheng Y, Chen Y, Wang Y, Xing J, Liu H, Xu Y, Lin Y, Pei Z, Wei X, Ding J, Li S, Wang K, Yao F, Zhao Y, Ding C, Hu W. Macrophage membrane-camouflaged biomimetic nanoparticles for rheumatoid arthritis treatment via modulating macrophage polarization. Journal Of Nanobiotechnology 2024, 22: 578. PMID: 39300463, PMCID: PMC11414146, DOI: 10.1186/s12951-024-02822-9.Peer-Reviewed Original ResearchConceptsCollagen-induced arthritisNanotherapeutic systemInflamed jointsRheumatoid arthritisMacrophage polarizationModulating macrophage polarizationDelay disease progressionDebilitating autoimmune diseaseChronic joint inflammationComprehensive in vitroAnti-inflammatory M2 phenotypeReduced synovial inflammationEnhanced cellular uptakeIntra-articular injectionRheumatoid arthritis treatmentPro-inflammatory M1Treatment optionsAutoimmune diseasesRepolarize macrophagesBiomimetic nanoparticlesDisease progressionMouse modelNanoparticlesTherapeutic strategiesSide effectsA spatial expression atlas of the adult human proximal small intestine
Harnik Y, Yakubovsky O, Hoefflin R, Novoselsky R, Bahar Halpern K, Barkai T, Korem Kohanim Y, Egozi A, Golani O, Addadi Y, Kedmi M, Keidar Haran T, Levin Y, Savidor A, Keren-Shaul H, Mayer C, Pencovich N, Pery R, Shouval D, Tirosh I, Nachmany I, Itzkovitz S. A spatial expression atlas of the adult human proximal small intestine. Nature 2024, 632: 1101-1109. PMID: 39112711, DOI: 10.1038/s41586-024-07793-3.Peer-Reviewed Original ResearchConceptsExpression atlasSingle-molecule fluorescence in situ hybridizationLipid droplet assemblyAdult human gutFluorescence in situ hybridizationHuman proximal small intestineHuman small intestineHuman gutSpatial proteomicsProximal small intestineTip cellsGene expressionSmall intestineIron uptakeSpatial transcriptomicsVillus tip cellsImmune cell typesMouse small intestineCell typesDroplet assemblyImmunosuppressive rolePro-immunogenicAdult human small intestineT cellsZonated expressionCTHRC1+ fibroblasts and SPP1+ macrophages synergistically contribute to pro-tumorigenic tumor microenvironment in pancreatic ductal adenocarcinoma
Li E, Cheung H, Ma S. CTHRC1+ fibroblasts and SPP1+ macrophages synergistically contribute to pro-tumorigenic tumor microenvironment in pancreatic ductal adenocarcinoma. Scientific Reports 2024, 14: 17412. PMID: 39075108, PMCID: PMC11286765, DOI: 10.1038/s41598-024-68109-z.Peer-Reviewed Original ResearchConceptsPancreatic ductal adenocarcinomaTumor-associated macrophagesTumor microenvironmentEpithelial mesenchymal transitionDuctal adenocarcinomaImmune-suppressive tumor microenvironmentPro-tumorigenic tumor microenvironmentPancreatic cancer casesHeterogeneous tumor microenvironmentCombination of single-cellCancer-associated myofibroblastsSurgical resectionMyeloid cellsCurrent therapiesCancer casesLethal cancersSurvival rateExtracellular matrixTreat cancerMesenchymal transitionTherapeutic targetAdenocarcinomaCellular populationsCancerIntercellular interactionsFrom metabolic to epigenetic: Insight into trained macrophages in atherosclerosis (Review)
Li T, Feng W, Yan W, Wang T. From metabolic to epigenetic: Insight into trained macrophages in atherosclerosis (Review). Molecular Medicine Reports 2024, 30: 145. PMID: 38904193, DOI: 10.3892/mmr.2024.13269.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAtherosclerosisEpigenesis, GeneticHumansImmunity, InnateMacrophagesPlaque, AtheroscleroticConceptsTrained immunityTrained macrophagesAbundant immune cellsCharacteristics of innate immunityChronic inflammatory diseaseAtherosclerotic plaquesProgression of ASImmune cellsInflammatory diseasesImmune responseTherapeutic approachesClinical strategiesEpigenetic reprogrammingDeposition of lipoproteinsCardiovascular diseaseInnate immunityMacrophagesAtherosclerosisImmunityDiseasePlaqueCellsComplex mechanismsNoninvasive assessment of the lung inflammation-fibrosis axis by targeted imaging of CMKLR1
Mannes P, Adams T, Farsijani S, Barnes C, Latoche J, Day K, Nedrow J, Ahangari F, Kaminski N, Lee J, Tavakoli S. Noninvasive assessment of the lung inflammation-fibrosis axis by targeted imaging of CMKLR1. Science Advances 2024, 10: eadm9817. PMID: 38896611, PMCID: PMC11186491, DOI: 10.1126/sciadv.adm9817.Peer-Reviewed Original ResearchConceptsIdiopathic pulmonary fibrosisFibrotic lung diseaseRisk stratificationMurine modelLung fibrosisLung diseaseModel of bleomycin-induced lung fibrosisBleomycin-induced lung fibrosisImaging biomarkersMurine model of bleomycin-induced lung fibrosisBronchoalveolar lavage cellsMonocyte-derived macrophagesPositron emission tomographyInflammatory endotypesPulmonary fibrosisLavage cellsPoor survivalNoninvasive assessmentTherapeutic monitoringEmission tomographyCMKLR1FibrosisClinical trajectoryLungLung regionsOverexpression of Malat1 drives metastasis through inflammatory reprogramming of the tumor microenvironment
Martinez-Terroba E, Plasek-Hegde L, Chiotakakos I, Li V, de Miguel F, Robles-Oteiza C, Tyagi A, Politi K, Zamudio J, Dimitrova N. Overexpression of Malat1 drives metastasis through inflammatory reprogramming of the tumor microenvironment. Science Immunology 2024, 9: eadh5462. PMID: 38875320, DOI: 10.1126/sciimmunol.adh5462.Peer-Reviewed Original ResearchConceptsTumor microenvironmentLung adenocarcinomaMetastatic diseasePromoting metastatic diseaseGlobal chromatin accessibilityMetastasis-associated lung adenocarcinoma transcript 1Overexpression of MALAT1Lung adenocarcinoma transcript 1Lung adenocarcinoma metastasisCCL2 blockadeInflammatory reprogrammingEnhanced cell mobilityMacrophage depletionMechanism of actionTumor typesTumor progressionMouse modelCell mobilizationTumorLong noncoding RNAsParacrine secretionMetastasisCell linesTranscript 1MicroenvironmentResident and recruited macrophages differentially contribute to cardiac healing after myocardial ischemia
Weinberger T, Denise M, Joppich M, Fischer M, Rodriguez C, Kumaraswami K, Wimmler V, Ablinger S, Räuber S, Fang J, Liu L, Liu H, Winterhalter J, Lichti J, Thomas L, Esfandyari D, Percin G, Matin S, Hidalgo A, Waskow C, Engelhardt S, Todica A, Zimmer R, Pridans C, Perdiguero E, Schulz C. Resident and recruited macrophages differentially contribute to cardiac healing after myocardial ischemia. ELife 2024, 12: rp89377. PMID: 38775664, PMCID: PMC11111219, DOI: 10.7554/elife.89377.Peer-Reviewed Original ResearchConceptsInfarct sizeCardiac remodelingI/R injuryMacrophage populationsDeterioration of cardiac functionRecruitment of monocyte-derived macrophagesIschemia/reperfusion (I/R) injuryAntigen-presenting macrophagesImmune cell crosstalkSubsets of macrophagesIncreased infarct sizeMonocyte-derived macrophagesResponse to injuryInfluence infarct sizeContext of myocardial infarctionCSF1R inhibitionCardiac healingCardiac macrophagesCardiac functionCell crosstalkAdverse remodelingResident macrophagesTissue macrophagesMacrophage lineageMyocardial ischemiaEnhancing in vivo cell and tissue targeting by modulation of polymer nanoparticles and macrophage decoys
Piotrowski-Daspit A, Bracaglia L, Eaton D, Richfield O, Binns T, Albert C, Gould J, Mortlock R, Egan M, Pober J, Saltzman W. Enhancing in vivo cell and tissue targeting by modulation of polymer nanoparticles and macrophage decoys. Nature Communications 2024, 15: 4247. PMID: 38762483, PMCID: PMC11102454, DOI: 10.1038/s41467-024-48442-7.Peer-Reviewed Original ResearchConceptsPoly(amine-co-esterPolymer nanoparticlesDelivery of nucleic acid therapeuticsCell-type tropismTissue tropismNucleic acid delivery vehiclesIn vivo deliveryIn vivo efficacyCirculation half-lifeNucleic acid therapeuticsVehicle characteristicsTunable propertiesBiodistribution assessmentPhysiological fatePolymer chemistrySurface propertiesPharmacokinetic modelTissue targetingNanoparticlesDistribution modifiersPolymeric nanoparticlesTropismPolymerDelivery vehiclesHalf-lifeKeratin 17 modulates the immune topography of pancreatic cancer
Delgado-Coka L, Horowitz M, Torrente-Goncalves M, Roa-Peña L, Leiton C, Hasan M, Babu S, Fassler D, Oentoro J, Bai J, Petricoin E, Matrisian L, Blais E, Marchenko N, Allard F, Jiang W, Larson B, Hendifar A, Chen C, Abousamra S, Samaras D, Kurc T, Saltz J, Escobar-Hoyos L, Shroyer K. Keratin 17 modulates the immune topography of pancreatic cancer. Journal Of Translational Medicine 2024, 22: 443. PMID: 38730319, PMCID: PMC11087249, DOI: 10.1186/s12967-024-05252-1.Peer-Reviewed Original ResearchConceptsPancreatic ductal adenocarcinomaCD8+ T cellsT cellsK17 expressionCell carcinomaPatient survivalMolecular subtypes of pancreatic ductal adenocarcinomaIntratumoral CD8+ T cellsSpatial distribution of T cellsKeratin 17CD8+ T cell abundanceImmune responseSubtype of pancreatic ductal adenocarcinomaCervical squamous cell carcinomaAssociated with decreased numbersCD16+ macrophagesTumor-intrinsic variablesDistribution of T cellsLymph node statusSquamous cell carcinomaBasal cell carcinomaCD163+ macrophagesT cell abundanceImmune cell responsesImmunotherapeutic opportunitiesNatural resistance to meglumine antimoniate is associated with treatment failure in cutaneous leishmaniasis caused by Leishmania (Viannia) panamensis
Fernández O, Rosales-Chilama M, Sánchez-Hidalgo A, Gómez P, Rebellón-Sánchez D, Regli I, Díaz-Varela M, Tacchini-Cottier F, Saravia N. Natural resistance to meglumine antimoniate is associated with treatment failure in cutaneous leishmaniasis caused by Leishmania (Viannia) panamensis. PLOS Neglected Tropical Diseases 2024, 18: e0012156. PMID: 38709850, PMCID: PMC11098511, DOI: 10.1371/journal.pntd.0012156.Peer-Reviewed Original ResearchConceptsAssociated with treatment failureTreatment failureHost risk factorsBALB/c miceRisk factorsDrug susceptibilityClinical strainsOutcome of cutaneous leishmaniasisOdds of treatment failureMeglumine antimoniateParasitological response to treatmentLeishmania (Viannia) panamensisSubgroup of patientsAntimicrobial drug susceptibilityResponse to treatmentU937 macrophagesEvaluate drug susceptibilityCutaneous leishmaniasis patientsCutaneous leishmaniasisFailed treatmentPlasma CmaxTherapeutic responseClinical outcomesPatient's lesionsTreatment outcomesSingle-cell transcriptomics reveal distinct immune-infiltrating phenotypes and macrophage–tumor interaction axes among different lineages of pituitary neuroendocrine tumors
Lin S, Dai Y, Han C, Han T, Zhao L, Wu R, Liu J, Zhang B, Huang N, Liu Y, Lai S, Shi J, Wang Y, Lou M, Xie J, Cheng Y, Tang H, Yao H, Fang H, Zhang Y, Wu X, Shen L, Ye Y, Xue L, Wu Z. Single-cell transcriptomics reveal distinct immune-infiltrating phenotypes and macrophage–tumor interaction axes among different lineages of pituitary neuroendocrine tumors. Genome Medicine 2024, 16: 60. PMID: 38658971, PMCID: PMC11040908, DOI: 10.1186/s13073-024-01325-4.Peer-Reviewed Original ResearchConceptsTumor immune microenvironmentTumor-associated macrophagesTumor cell apoptosisTumor cellsImmune cellsNeuroendocrine tumorsQuantitative immunofluorescenceComposition of immune cellsInfiltration of immune cellsMultiplexed quantitative immunofluorescenceLevel of immune infiltrationScRNA-seqPituitary neuroendocrine tumorsCX3CR1+ macrophagesDiversity of tumorsCell apoptosisSignificance of macrophagesRNA sequencing samplesScRNA-seq dataCX3CR1+Subcutaneous xenograft experimentsImmune microenvironmentSingle-cell RNA sequencingImmunological environmentImmune infiltrationThe crosstalk between macrophages and cancer cells potentiates pancreatic cancer cachexia
Liu M, Ren Y, Zhou Z, Yang J, Shi X, Cai Y, Arreola A, Luo W, Fung K, Xu C, Nipp R, Bronze M, Zheng L, Li Y, Houchen C, Zhang Y, Li M. The crosstalk between macrophages and cancer cells potentiates pancreatic cancer cachexia. Cancer Cell 2024, 42: 885-903.e4. PMID: 38608702, PMCID: PMC11162958, DOI: 10.1016/j.ccell.2024.03.009.Peer-Reviewed Original ResearchConceptsPancreatic cancer cachexiaTumor cellsCancer cachexiaTherapeutic targetLimited treatment optionsPancreatic cancer cellsImmune microenvironmentCCL2/CCR2 axisPotential therapeutic targetTreatment optionsMuscle wastingReprogram macrophagesTumorMuscle atrophyCachexiaCancer cellsMacrophagesNon-autonomous activationMuscle remodelingCancerMuscle degradationSecretionCellsMuscleTWEAK
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