2025
FGF21 Signaling Exerts Antifibrotic Properties during Pulmonary Fibrosis.
Ghanem M, Archer G, Justet A, Jaillet M, Vasarmidi E, Mordant P, Castier Y, Mal H, Cazes A, Poté N, Crestani B, Mailleux A. FGF21 Signaling Exerts Antifibrotic Properties during Pulmonary Fibrosis. American Journal Of Respiratory And Critical Care Medicine 2025, 211: 486-498. PMID: 39637324, DOI: 10.1164/rccm.202311-2021oc.Peer-Reviewed Original ResearchConceptsIdiopathic pulmonary fibrosisWild-type littermatesPlasma of patientsPulmonary fibrosisAntifibrotic propertiesIntratracheal injection of bleomycinDevelopment of pulmonary fibrosisDecreased fibrosis markersEffects of FGF21Increased sensitivity to bleomycinInjection of bleomycinPulmonary fibrosis developmentSensitivity to bleomycinDecrease of BaxConcentrations of FGF21Human lung fibroblastsTherapeutic optionsFibrosis markersAntifibrotic effectsControl subjectsInjury scoreIntratracheal injectionLiver fibrosisLung fibrogenesisFibroblast growth factorCD103+ dendritic cell — fibroblast crosstalk via TLR9, TDO2, and AHR signaling drives lung fibrogenesis
Carter H, Costa R, Adams T, Gilchrist T, Emch C, Bame M, Oldham J, Huang S, Linderholm A, Noth I, Kaminski N, Moore B, Gurczynski S. CD103+ dendritic cell — fibroblast crosstalk via TLR9, TDO2, and AHR signaling drives lung fibrogenesis. JCI Insight 2025, 10 PMID: 39964756, PMCID: PMC11949071, DOI: 10.1172/jci.insight.177072.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntigens, CDBasic Helix-Loop-Helix Transcription FactorsBleomycinDendritic CellsDisease Models, AnimalFibroblastsHumansIdiopathic Pulmonary FibrosisIntegrin alpha ChainsInterleukin-6LungMaleMiceMice, Inbred C57BLReceptors, Aryl HydrocarbonSignal TransductionToll-Like Receptor 9Tryptophan OxygenaseConceptsIdiopathic pulmonary fibrosisAhR signalingMice treated with BLMIL-17+ cellsCD103+ DCLoss of lung functionStudies of human samplesLimited treatment optionsTreated ex vivoProduction of IL-6Inflammatory cytokine productionExon 2 deletionExpression of TDO2IL-6 productionAdoptive transferCD11c-CreCD11c+ cellsImmunological changesPulmonary fibrosisTLR agonistsProgressive scarringTreatment optionsCytokine productionLung fibrogenesisAryl hydrocarbon receptorMulti-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 ResearchAn Injectable Alginate Hydrogel Modified by Collagen and Fibronectin for Better Cellular Environment
Gao D, Shipman W, Sun Y, Yang W, Mathew A, Beraki L, Glahn J, Kochen A, Kyriakides T, Horsley V, Hsia H. An Injectable Alginate Hydrogel Modified by Collagen and Fibronectin for Better Cellular Environment. ACS Applied Bio Materials 2025, 8: 1675-1683. PMID: 39886738, DOI: 10.1021/acsabm.4c01853.Peer-Reviewed Original ResearchConceptsEncapsulated fibroblastsAlginate hydrogelNeat alginate hydrogelsComposite hydrogelsModified hydrogelsInjectable hydrogelsStorage modulusMechanical propertiesCollagen hydrogelsMacroporous structureHydrogelsPore sizeAlginate functionalizationAlginate controlAlginate matrixAlginateFibroblast behaviorPro-angiogenic potentialFibroblast spreadingModulusPromote wound healingPoreFormation of fibrilsSLC10A7 regulates O-GalNAc glycosylation and Ca2+ homeostasis in the secretory pathway: insights into SLC10A7-CDG
Durin Z, Layotte A, Morelle W, Houdou M, Folcher A, Legrand D, Lefeber D, Prevarskaya N, Von Blume J, Cormier-Daire V, Foulquier F. SLC10A7 regulates O-GalNAc glycosylation and Ca2+ homeostasis in the secretory pathway: insights into SLC10A7-CDG. Cellular And Molecular Life Sciences 2025, 82: 40. PMID: 39779512, PMCID: PMC11711720, DOI: 10.1007/s00018-024-05551-2.Peer-Reviewed Original ResearchConceptsCongenital disorders of glycosylationGlycan synthesisCa2+ homeostasisGolgi glycosylation defectsO-GalNAc glycosylationO-glycosylation defectRegulation of Ca2+ homeostasisGolgi transmembrane proteinCongenital disorders of glycosylation patientsDisorders of glycosylationGolgi homeostasisGolgi localizationGolgi compartmentSecretory pathwayHAP1 cellsProtein familyPatient fibroblastsGlycosylation defectsTransmembrane proteinsGalNAc residuesTransporter familyTight regulationGolgiGlycosylation abnormalitiesSLC10A7
2024
Targeting hypoxia and thrombospondin‐2 in diabetic wound healing
Huang Y, Xing H, Naud S, Kyriakides T. Targeting hypoxia and thrombospondin‐2 in diabetic wound healing. The FASEB Journal 2024, 38: e70091. PMID: 39383062, PMCID: PMC11486302, DOI: 10.1096/fj.202302429rrr.Peer-Reviewed Original ResearchConceptsThrombospondin-2Diabetic miceWound healingHIF-1aMatricellular protein thrombospondin-2Diabetic woundsImpaired wound healingWounds of diabetic miceDimethyloxalylglycine treatmentTargeting hypoxiaSustained hypoxiaDiabetic patientsTSP2 expressionCell dysfunctionIncreased neovascularizationDiabetic wound healingGenetic ablationDiabetic fibroblastsElevated glucoseReduced hypoxiaImprove healingImmunofluorescence analysisHIF-1a activationHypoxiaWestern blottingCC2D1A causes ciliopathy, intellectual disability, heterotaxy, renal dysplasia, and abnormal CSF flow
Kim A, Sakin I, Viviano S, Tuncel G, Aguilera S, Goles G, Jeffries L, Ji W, Lakhani S, Kose C, Silan F, Oner S, Kaplan O, Group M, Ergoren M, Mishra-Gorur K, Gunel M, Sag S, Temel S, Deniz E. CC2D1A causes ciliopathy, intellectual disability, heterotaxy, renal dysplasia, and abnormal CSF flow. Life Science Alliance 2024, 7: e202402708. PMID: 39168639, PMCID: PMC11339347, DOI: 10.26508/lsa.202402708.Peer-Reviewed Original ResearchConceptsDevelopmental disabilitiesIntellectual disabilityPatient-derived fibroblastsMidbrain regionsBrain developmentDefective ciliogenesisCSF circulationDisabilityCSF flowAbnormal CSF flowNervous system developmentMutant tadpolesCiliated tissuesMultiple model systemsVariant functionPronephric ductUnrelated familiesCC2D1AExpression patternsCiliogenesisRenal dysplasiaLeft-right organizerFunctional analysisDisease mechanismsBrainCTHRC1+ 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 interactionsOverlapping role of synaptophysin and synaptogyrin family proteins in determining the small size of synaptic vesicles
Park D, Fujise K, Wu Y, Luján R, Del Olmo-Cabrera S, Wesseling J, De Camilli P. Overlapping role of synaptophysin and synaptogyrin family proteins in determining the small size of synaptic vesicles. Proceedings Of The National Academy Of Sciences Of The United States Of America 2024, 121: e2409605121. PMID: 38985768, PMCID: PMC11260120, DOI: 10.1073/pnas.2409605121.Peer-Reviewed Original ResearchConceptsSynaptic vesiclesFamily proteinsBiogenesis of synaptic vesiclesClusters of small vesiclesSize of synaptic vesiclesSynaptogyrin familySynaptogyrin-1Vesicle proteinsSynaptogyrinTransmembrane domainOrganismal levelSmall vesiclesProteinMild defectsVesiclesFamily membersBiogenesisSmall sizeFamilyMiceSynapsinCoexpressionAbundanceSynaptoporinMembersBone marrow mesenchymal stem cell-derived exosomes shuttle microRNAs to endometrial stromal fibroblasts that promote tissue proliferation /regeneration/ and inhibit differentiation
Bonavina G, Mamillapalli R, Krikun G, Zhou Y, Gawde N, Taylor H. Bone marrow mesenchymal stem cell-derived exosomes shuttle microRNAs to endometrial stromal fibroblasts that promote tissue proliferation /regeneration/ and inhibit differentiation. Stem Cell Research & Therapy 2024, 15: 129. PMID: 38693588, PMCID: PMC11064399, DOI: 10.1186/s13287-024-03716-1.Peer-Reviewed Original ResearchConceptsMiR-100-5pMiR-100MiR-21Transmission electron microscopyMiR-143MiR-143-3pMiR-21-5pEndometrial stromal fibroblastsStromal fibroblastsMicroRNAsExtracellular vesiclesElectron microscopyCell-free regenerative therapyNanoparticle tracking analysisMiRNAsBone marrow mesenchymal stem cell-derived exosomesBone marrow-derived stem cellsMesenchymal stem cell-derived exosomesStem cell-derived exosomesDelivery of microRNAsMarrow-derived stem cellsAssociated with several signaling pathwaysMediators of tissue repairMethodsExtracellular vesiclesUnpaired t-testTANGO1 inhibitors reduce collagen secretion and limit tissue scarring
Raote I, Rosendahl A, Häkkinen H, Vibe C, Küçükaylak I, Sawant M, Keufgens L, Frommelt P, Halwas K, Broadbent K, Cunquero M, Castro G, Villemeur M, Nüchel J, Bornikoel A, Dam B, Zirmire R, Kiran R, Carolis C, Andilla J, Loza-Alvarez P, Ruprecht V, Jamora C, Campelo F, Krüger M, Hammerschmidt M, Eckes B, Neundorf I, Krieg T, Malhotra V. TANGO1 inhibitors reduce collagen secretion and limit tissue scarring. Nature Communications 2024, 15: 3302. PMID: 38658535, PMCID: PMC11043333, DOI: 10.1038/s41467-024-47004-1.Peer-Reviewed Original ResearchConceptsEndoplasmic reticulum exit sitesECM proteinsSecretion of ECM proteinsPeptide inhibitorFibrotic diseasesCollagen exportTANGO1Binding interfaceWound healingZebrafish resultsECM componentsReduced granulation tissue formationGranulation tissue formationEffective therapyCutaneous wound healingInhibitor treatmentFibrotic processUncontrolled secretionWidespread occurrenceProtein levelsExit siteExcessive scarringAmount of collagenTherapeutic modulationTissue scarringTRPM7 facilitates fibroblast-like synoviocyte proliferation, metastasis and inflammation through increasing IL-6 stability via the PKCα-HuR axis in rheumatoid arthritis
Lin Y, Chen Y, Hu W, Liu X, Hao W, Xing J, Ding J, Xu Y, Yao F, Zhao Y, Wang K, Li S, Yu Q, Hu W, Zhou R. TRPM7 facilitates fibroblast-like synoviocyte proliferation, metastasis and inflammation through increasing IL-6 stability via the PKCα-HuR axis in rheumatoid arthritis. International Immunopharmacology 2024, 132: 111933. PMID: 38581988, DOI: 10.1016/j.intimp.2024.111933.Peer-Reviewed Original ResearchConceptsTransient receptor potential melastatin 7Rheumatoid arthritisInhibition of transient receptor potential melastatin 7Human RA patientsSynovial hyperplasiaAdjuvant-induced arthritis ratsIncreased TRPM7 expressionIL-6 mRNATreatment of RAPathogenesis of RAFibroblast-like synoviocytesTRPM7 silencingProgression of rheumatoid arthritisTRPM7 expressionChannel inhibitionCation channelsRA patientsMetastasisPharmacological inhibitionArthritis ratsInflammationNuclear translocationSynoviocyte proliferationHyperplasiaProliferationCharting the cellular biogeography in colitis reveals fibroblast trajectories and coordinated spatial remodeling
Cadinu P, Sivanathan K, Misra A, Xu R, Mangani D, Yang E, Rone J, Tooley K, Kye Y, Bod L, Geistlinger L, Lee T, Mertens R, Ono N, Wang G, Sanmarco L, Quintana F, Anderson A, Kuchroo V, Moffitt J, Nowarski R. Charting the cellular biogeography in colitis reveals fibroblast trajectories and coordinated spatial remodeling. Cell 2024, 187: 2010-2028.e30. PMID: 38569542, PMCID: PMC11017707, DOI: 10.1016/j.cell.2024.03.013.Peer-Reviewed Original ResearchConceptsMultiplexed error-robust fluorescence in situ hybridizationFluorescence in situ hybridizationSpatial organizationCell-cell interactionsDiverse cell populationsHealthy gutMouse colitis modelExpression profilesBiogeographyGutNon-immune cellsGut inflammationSpatial remodelingInflammation-associated fibroblastsTissue neighborhoodsInflammation-induced remodelingCell populationsFibroblastsImmune cellsCellsColitis modelUlcerative colitisFibroblastic originStage progressionExpressionExtracellular CIRP induces abnormal activation of fibroblast-like synoviocytes from patients with RA via the TLR4-mediated HDAC3 pathways
Yao F, Zhao Y, Yu Q, Hu W, Lin Y, Chen Y, Li L, Sun C, Li S, Wang K, Yang M, Zhou R, Hu W. Extracellular CIRP induces abnormal activation of fibroblast-like synoviocytes from patients with RA via the TLR4-mediated HDAC3 pathways. International Immunopharmacology 2024, 128: 111525. PMID: 38218010, DOI: 10.1016/j.intimp.2024.111525.Peer-Reviewed Original ResearchConceptsExtracellular cold-inducible RNA-binding proteinCold-inducible RNA-binding proteinToll-like receptor 4Histone deacetylase 3Endogenous proinflammatory moleculesRheumatoid arthritisActivity of RA-FLSAA ratsAbnormal activationProinflammatory moleculesEffect of cold-inducible RNA-binding proteinHistone deacetylase 3 knockdownRelease of IL-1bSeverity of arthritisFibroblast-like synoviocytesDevelopment of rheumatoid arthritisRA-FLSActivation of fibroblast-like synoviocytesIL-33Expression of N-cadherinProinflammatory effectsArthritis severityIL-1BInflammatory diseasesReceptor 4
2023
Apoptosis recognition receptors regulate skin tissue repair in mice
Justynski O, Bridges K, Krause W, Forni M, Phan Q, Sandoval-Schaefer T, Carter K, King D, Hsia H, Gazes M, Vyce S, Driskell R, Miller-Jensen K, Horsley V. Apoptosis recognition receptors regulate skin tissue repair in mice. ELife 2023, 12: e86269. PMID: 38127424, PMCID: PMC10735221, DOI: 10.7554/elife.86269.Peer-Reviewed Original ResearchShort- and long-term effects of radiation exposure at low dose and low dose rate in normal human VH10 fibroblasts
Akuwudike P, López-Riego M, Marczyk M, Kocibalova Z, Brückner F, Polańska J, Wojcik A, Lundholm L. Short- and long-term effects of radiation exposure at low dose and low dose rate in normal human VH10 fibroblasts. Frontiers In Public Health 2023, 11: 1297942. PMID: 38162630, PMCID: PMC10755029, DOI: 10.3389/fpubh.2023.1297942.Peer-Reviewed Original ResearchMeSH KeywordsDose-Response Relationship, RadiationFibroblastsGamma RaysHumansRadiation ExposureRadiation, IonizingConceptsLong-term effectsLow dosesDose-rate effectiveness factorLow dose rateSignificant early effectsColony forming assaysDays post irradiationEarly time pointsPooled cohortValidation cohortStrong cytotoxic effectEpidemiological dataLow doseGy/minCell growth curveSample cohortCohortThird cohortCell viability assaysRadiation exposureEarly effectsTime pointsCytotoxic effectsGene expression changesConsistent upregulationFibroblast activation protein: Pivoting cancer/chemotherapeutic insight towards heart failure
Gehris J, Ervin C, Hawkins C, Womack S, Churillo A, Doyle J, Sinusas A, Spinale F. Fibroblast activation protein: Pivoting cancer/chemotherapeutic insight towards heart failure. Biochemical Pharmacology 2023, 219: 115914. PMID: 37956895, PMCID: PMC10824141, DOI: 10.1016/j.bcp.2023.115914.Peer-Reviewed Original ResearchMeSH KeywordsExtracellular MatrixFibroblastsHeart FailureHumansMyocardiumNeoplasmsVentricular RemodelingConceptsFibroblast activation proteinExtracellular matrixCancer progressionFibroblast subtypesProtein signaturesECM structureEnzyme pathwaysActivation proteinTherapeutic targetImportant mechanismFibroblastsProliferationFibroblast growthProteinProgressionPathwayRemodelingFunctionCancerDiscoveryChemotherapeuticsIncreased expression of CXCL6 in secretory cells drives fibroblast collagen synthesis and is associated with increased mortality in idiopathic pulmonary fibrosis
Bahudhanapati H, Tan J, Apel R, Seeliger B, Schupp J, Li X, Sullivan D, Sembrat J, Rojas M, Tabib T, Valenzi E, Lafyatis R, Mitash N, Pineda R, Jawale C, Peroumal D, Biswas P, Tedrow J, Adams T, Kaminski N, Wuyts W, McDyer J, Gibson K, Alder J, Königshoff M, Zhang Y, Nouraie M, Prasse A, Kass D. Increased expression of CXCL6 in secretory cells drives fibroblast collagen synthesis and is associated with increased mortality in idiopathic pulmonary fibrosis. European Respiratory Journal 2023, 63: 2300088. PMID: 37918852, DOI: 10.1183/13993003.00088-2023.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBleomycinChemokine CXCL6ChemokinesCollagenFibroblastsHumansIdiopathic Pulmonary FibrosisLungMiceConceptsIdiopathic pulmonary fibrosisAirway epithelial cellsBronchoalveolar lavagePulmonary fibrosisEpithelial cellsCollagen synthesisPathogenesis of IPFCohort of patientsIPF lung fibroblastsEffects of chemokinesAir-liquid interface culturesExpression of CXCL6Collagen I levelsIPF mortalityIPF patientsChemokine levelsIPF fibroblastsPoor survivalDistal lungI levelsWhole lungAnimal modelsEctopic localisationPatientsSingle-cell RNA sequencingSRC and TKS5 mediated podosome formation in fibroblasts promotes extracellular matrix invasion and pulmonary fibrosis
Barbayianni I, Kanellopoulou P, Fanidis D, Nastos D, Ntouskou E, Galaris A, Harokopos V, Hatzis P, Tsitoura E, Homer R, Kaminski N, Antoniou K, Crestani B, Tzouvelekis A, Aidinis V. SRC and TKS5 mediated podosome formation in fibroblasts promotes extracellular matrix invasion and pulmonary fibrosis. Nature Communications 2023, 14: 5882. PMID: 37735172, PMCID: PMC10514346, DOI: 10.1038/s41467-023-41614-x.Peer-Reviewed Original ResearchConceptsPulmonary fibrosisExtracellular matrix invasionLung fibroblastsIdiopathic pulmonary fibrosis patientsIdiopathic pulmonary fibrosisPulmonary fibrosis patientsMatrix invasionPromising therapeutic optionProfibrotic milieuTherapeutic optionsLung tissuePathogenic hallmarkPharmacological targetingFibrosisFibrosis patientsIncurable diseaseEx vivoBleomycinExtracellular matrix componentsTks5 expressionAberrant depositionInvasionMiceFibroblastsSrc kinaseFibroblasts – the cellular choreographers of wound healing
Knoedler S, Broichhausen S, Guo R, Dai R, Knoedler L, Kauke-Navarro M, Diatta F, Pomahac B, Machens H, Jiang D, Rinkevich Y. Fibroblasts – the cellular choreographers of wound healing. Frontiers In Immunology 2023, 14: 1233800. PMID: 37646029, PMCID: PMC10461395, DOI: 10.3389/fimmu.2023.1233800.Peer-Reviewed Original ResearchConceptsFibroblast diversityInnate immune cellsNovel treatment modalitiesWound healing functionsFascial connective tissueRole of fibroblastsTreatment modalitiesImmune cellsWound repairScar tissueDiversityFibroblastsConnective tissueHealing processWound healingComprehensive understandingMachineryTissueHealing functionCascade
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