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
2026
Collagen II hydrogel-mediated sustained delivery of lacosamide attenuates cartilage degeneration and pain in osteoarthritis
He C, Huang G, Moradi L, Bi J, Yang X, Liu X, Cui X, Varthi A, Wiznia D, Waxman S, Fu W, Liu C. Collagen II hydrogel-mediated sustained delivery of lacosamide attenuates cartilage degeneration and pain in osteoarthritis. Bioactive Materials 2026, 61: 640-656. PMID: 41799961, PMCID: PMC12963906, DOI: 10.1016/j.bioactmat.2026.02.045.Peer-Reviewed Original ResearchDisease-modifying therapiesIntra-articular deliveryIntra-articular administrationCartilage degenerationTranslational potentialOpen field testSodium channel inhibitorsSustained deliveryThermoresponsive hydrogelPain behaviorCartilage explantsClinical efficacyChannel inhibitorsTherapeutic durabilityLacosamideNav1.7 inhibitorsPainEquivalent doseChondrocyte metabolismClinical translationTherapyTherapeutic targetGene expression analysisHydrogelsDelivery strategiesA progranulin derivative blocks the C5a/C5aR1 signaling and mitigates pathology in Gaucher disease
Zhao X, Fu W, Lin Y, Liou B, Fannin V, Grabowski G, Sun Y, Liu C. A progranulin derivative blocks the C5a/C5aR1 signaling and mitigates pathology in Gaucher disease. Molecular Genetics And Metabolism 2026, 147: 109683. DOI: 10.1016/j.ymgme.2025.109683.Peer-Reviewed Original ResearchcPLA2 in musculoskeletal and autoimmune diseases: Molecular mechanisms and therapeutic insights
He C, Huang G, Bi J, Fu W, Liu C. cPLA2 in musculoskeletal and autoimmune diseases: Molecular mechanisms and therapeutic insights. Cytokine & Growth Factor Reviews 2026, 88: 18-31. PMID: 41512597, DOI: 10.1016/j.cytogfr.2026.01.002.Peer-Reviewed Original ResearchConceptsCytosolic phospholipase A2Regulators of lipid signalingCentral regulatorMAPK-mediated phosphorylationAutoimmune diseasesCell type-specific actionsImmune cell activationMechanistic overviewCytosolic phospholipase A2 activityGene editing approachesDuchenne muscular dystrophyMembrane translocationInflammatory bowel diseaseArachidonic acid metabolismExtracellular matrix turnoverSmall molecule inhibitorsDisease-modifying therapiesMitochondrial dysfunctionInflammatory myopathiesMolecular mechanismsIntervertebral disc degenerationAcid metabolismAutoimmune disordersImmune cellsLipid signaling
2025
Cytosolic phospholipase A2 as a therapeutic target for degenerative joint diseases
Huang G, He C, Fu W, Bi J, Wang J, Wiznia D, Liu C. Cytosolic phospholipase A2 as a therapeutic target for degenerative joint diseases. Bone Research 2025, 13: 86. PMID: 41093854, PMCID: PMC12528370, DOI: 10.1038/s41413-025-00470-9.Peer-Reviewed Original ResearchConceptsCytosolic phospholipase A2Intervertebral disc degenerationCartilage degenerationPharmacological inhibitionCytosolic phospholipase A2 inhibitorCytosolic phospholipase A2 expressionDegeneration of cartilaginous tissueTherapeutic targetDegenerative conditionsElevated levelsDegenerative musculoskeletal disordersDisease-modifying therapiesIntervertebral disc degeneration modelPhospholipase A2Over-the-counter drugsGenetic deletionMouse modelReduce inflammationSingle-cell RNA sequencingOver-the-counterDisc degenerationInflammationCartilage integrityTherapeutic potentialAge-relatedTNFR1-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, PMCID: PMC12374755, 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 target
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