Wenyu Fu
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Nav1.7 as a chondrocyte regulator and therapeutic target for osteoarthritis
Fu W, Vasylyev D, Bi Y, Zhang M, Sun G, Khleborodova A, Huang G, Zhao L, Zhou R, Li Y, Liu S, Cai X, He W, Cui M, Zhao X, Hettinghouse A, Good J, Kim E, Strauss E, Leucht P, Schwarzkopf R, Guo E, Samuels J, Hu W, Attur M, Waxman S, Liu C. Nav1.7 as a chondrocyte regulator and therapeutic target for osteoarthritis. Nature 2024, 625: 557-565. PMID: 38172636, PMCID: PMC10794151, DOI: 10.1038/s41586-023-06888-7.Peer-Reviewed Original ResearchVoltage-gated sodium channelsOA progressionDorsal root ganglion neuronsStructural joint damagePain relief treatmentHuman OA chondrocytesCommon joint diseaseMultiple mouse modelsNav1.7 blockersPain behaviorGanglion neuronsPharmacological blockadeJoint damageJoint degenerationChannel blockersJoint diseaseOA chondrocytesMouse modelTherapeutic targetOsteoarthritisIntracellular Ca2Nav1.7Nav1.7 channelsGenetic ablationLimited evidenceTNFR2/14-3-3ε signaling complex instructs macrophage plasticity in inflammation and autoimmunity
Fu W, Hu W, Yi Y, Hettinghouse A, Sun G, Bi Y, He W, Zhang L, Gao G, Liu J, Toyo-oka K, Xiao G, Solit D, Loke P, Liu C. TNFR2/14-3-3ε signaling complex instructs macrophage plasticity in inflammation and autoimmunity. Journal Of Clinical Investigation 2021, 131 PMID: 34185706, PMCID: PMC8363273, DOI: 10.1172/jci144016.Peer-Reviewed Original ResearchConceptsMacrophage polarizationMacrophage plasticityPI3K/Akt/mTORPathogenesis of inflammationMyeloid-specific deletionNF-κB activationAkt/mTORInflammatory arthritisAntiinflammatory pathwayImmunoregulatory roleAutoimmune diseasesProtective effectTherapeutic implicationsInflammationTNFR2 signalingAutoimmunityTNFR2TNFR2 activationReceptor complexDiseaseIntracellular regulatorsActivationMolecule 14TNFR1Arthritis14-3-3 epsilon is an intracellular component of TNFbib2 receptor complex and its activation protects against osteoarthritis
Fu W, Hettinghouse A, Chen Y, Hu W, Ding X, Chen M, Ding Y, Mundra J, Song W, Liu R, Yi Y, Attur M, Samuels J, Strauss E, Leucht P, Schwarzkopf R, Liu C. 14-3-3 epsilon is an intracellular component of TNFbib2 receptor complex and its activation protects against osteoarthritis. Annals Of The Rheumatic Diseases 2021, 80: 1615-1627. PMID: 34226187, PMCID: PMC8595573, DOI: 10.1136/annrheumdis-2021-220000.Peer-Reviewed Original ResearchConceptsPathogenesis of osteoarthritisTNFR2 complexTherapeutic effectSingle-cell RNA-seqIntracellular componentsReceptor complexExtracellular signal-regulated kinaseNuclear factor kappa BSignal-regulated kinaseCommon joint diseaseFactor kappa BChondrocyte-specific deletionProteomic screenElk-1RNA-seqTranscription factorsCell-based assaysTNF signalingTNFR2 pathwayInducible componentJoint diseaseActivity screenTherapeutic targetKappa BOsteoarthritis
2025
TNFR1-mediated senescence and lack of TNFR2-signaling limit human intervertebral disc cell repair potential in degenerative conditions
Gansau J, Grossi E, Rodriguez L, Wang M, Laudier D, Chaudhary S, Hecht A, Fu W, Sebra R, Liu C, Iatridis J. TNFR1-mediated senescence and lack of TNFR2-signaling limit human intervertebral disc cell repair potential in degenerative conditions. Osteoarthritis And Cartilage 2025, 33: 874-887. PMID: 40139648, PMCID: PMC12146073, DOI: 10.1016/j.joca.2025.02.791.Peer-Reviewed Original ResearchMeSH KeywordsAdultAgedAnnulus FibrosusCells, CulturedCellular SenescenceCulture Media, ConditionedFemaleHumansIntervertebral DiscIntervertebral Disc DegenerationMaleMiddle AgedReceptors, Tumor Necrosis Factor, Type IReceptors, Tumor Necrosis Factor, Type IISignal TransductionTumor Necrosis Factor-alphaConceptsTNFR2 signalingConditioned mediumInflammatory responseIVD cellsHuman annulus fibrosusDelivery of macrophagesPainful intervertebral discIntervertebral discAttenuated inflammatory responsePro-inflammatory responseNo effectHuman IVD cellsHuman annulus fibrosus cellsReduced metabolic rateReceptor 2Cytokine mixtureMacrophage populationsHAFS cellsInflammatory proteinsMetabolic impairmentBulk RNA-seqIntervertebral disc repairMetabolic rateCell cycle stateAutopsy subjectsTau is a receptor with low affinity for glucocorticoids and is required for glucocorticoid-induced bone loss
Fu W, Chen M, Wang K, Chen Y, Cui Y, Xie Y, Lei Z, Hu W, Sun G, Huang G, He C, Fretz J, Hettinghouse A, Liu R, Cai X, Zhang M, Chen Y, Jiang N, He M, Wiznia D, Xu H, Chen Z, Chen L, Tang K, Zhou H, Liu C. Tau is a receptor with low affinity for glucocorticoids and is required for glucocorticoid-induced bone loss. Cell Research 2025, 35: 23-44. PMID: 39743632, PMCID: PMC11701132, DOI: 10.1038/s41422-024-01016-0.Peer-Reviewed Original ResearchConceptsGC-induced osteoporosisBone lossInflammatory arthritisAdverse effects of dexamethasoneGlucocorticoid-induced bone lossHigh-dose dexamethasoneEffect of dexamethasoneFDA-approved drug librarySynthetic GCTreat inflammatory arthritisImmunosuppressive drugsPrescribed anti-inflammatoryGC receptorCombinatorial administrationSide effectsLow affinityGlucocorticoidOsteoporosisDexamethasoneReceptorsAdverse effectsBinding receptorsAnti-inflammatoryDrug libraryTau deficiency
2024
Ion channels in osteoarthritis: emerging roles and potential targets
Zhou R, Fu W, Vasylyev D, Waxman S, Liu C. Ion channels in osteoarthritis: emerging roles and potential targets. Nature Reviews Rheumatology 2024, 20: 545-564. PMID: 39122910, DOI: 10.1038/s41584-024-01146-0.Peer-Reviewed Original ResearchIon channelsVoltage-dependent calcium channelsAcid-sensing ion channelsTransient receptor potential channelsVoltage-gated sodium channelsIon channel modulatorsFunction of ion channelsPotential clinical applicationsCalcium channelsPreclinical studiesClinical impactSymptomatic reliefPotassium channelsChloride channelsDisease-modifying treatmentsClinical trialsSodium channelsBone hyperplasiaChannel modulationIon channel biologySynovial inflammationClinical applicationPiezo channelsModel of OAPotential targetProgranulin deficiency associates with postmenopausal osteoporosis via increasing ubiquitination of estrogen receptor α
Li G, Wang A, Tang W, Fu W, Tian Q, Jian J, Lata M, Hettinghouse A, Ding Y, Wei J, Zhao X, Wang M, Dong Q, Liu C, Xu Y. Progranulin deficiency associates with postmenopausal osteoporosis via increasing ubiquitination of estrogen receptor α. Genes & Diseases 2024, 12: 101221. PMID: 39559258, PMCID: PMC11570241, DOI: 10.1016/j.gendis.2024.101221.Peer-Reviewed Original ResearchPostmenopausal osteoporosisEstrogen receptorReceptor AEstrogen signalingTreatment of postmenopausal osteoporosisOvariectomy-induced bone lossEstrogen-mediated inhibitionRegulation of bone mineral densityBone mineral densityEstrogen receptor aPGRN-deficient miceInhibition of osteoclastogenesisPostmenopausal womenEstrogen deficiencyMineral densityLoss of progranulinEstrogen regulationBone lossBone massPositive feedback regulatory loopBone resorptionOsteoporosisTherapeutic approachesEstrogenOsteoporosis model
2023
Unraveling the mechanisms behind joint damage
Fu W, Liu C. Unraveling the mechanisms behind joint damage. ELife 2023, 12: e89778. PMID: 37366155, PMCID: PMC10299819, DOI: 10.7554/elife.89778.Peer-Reviewed Original ResearchPathogenic mechanisms of glucocorticoid-induced osteoporosis
Chen M, Fu W, Xu H, Liu C. Pathogenic mechanisms of glucocorticoid-induced osteoporosis. Cytokine & Growth Factor Reviews 2023, 70: 54-66. PMID: 36906448, PMCID: PMC10518688, DOI: 10.1016/j.cytogfr.2023.03.002.Peer-Reviewed Original ResearchConceptsGlucocorticoid-induced osteoporosisExogenous glucocorticoidsGC excessBone cellsBone formationImpaired bone formationMultiple adverse effectsLong-term useExcessive glucocorticoidsAutoimmune diseasesBone resorptionPrescribed medicinesEnhanced osteoclastogenesisPathogenic mechanismsProcess of osteoblastogenesisGlucocorticoidsHigh dosesOsteoclast apoptosisApoptosis of osteoblastsMature osteoclastsAdverse effectsOsteoclastsDifferentiation of osteoblastsOsteoporosisOsteoclastogenesisTau deficiency inhibits classically activated macrophage polarization and protects against collagen-induced arthritis in mice
Chen M, Fu W, Xu H, Liu C. Tau deficiency inhibits classically activated macrophage polarization and protects against collagen-induced arthritis in mice. Arthritis Research & Therapy 2023, 25: 146. PMID: 37559125, PMCID: PMC10410869, DOI: 10.1186/s13075-023-03133-4.Peer-Reviewed Original ResearchConceptsInflammatory cell infiltrationPro-inflammatory cytokinesRheumatoid arthritisAnkle jointSerum levelsCell infiltrationMacrophage polarizationOsteoclast activityCartilage damagePathogenesis of RACollagen-induced arthritis modelTau-/- miceCollagen-induced arthritisInflammatory joint diseasePro-inflammatory functionsProgression of CIAPotential therapeutic targetRole of tauInflammatory arthritisBone erosionArthritis incidenceBone lossClinical scoresArthritis modelInflammatory disorders
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