2025
Biomarkers in Autosomal Dominant Tubulointerstitial Kidney Disease
Li M, Jiang L, Liu Z, You R, Li Y, Xiang C, Yang L, Zhang H, Zhou X. Biomarkers in Autosomal Dominant Tubulointerstitial Kidney Disease. Integrative Medicine In Nephrology And Andrology 2025, 12 DOI: 10.1097/imna-d-24-00050.Peer-Reviewed Original ResearchAutosomal dominant tubulointerstitial kidney diseaseChronic kidney diseaseTubulointerstitial kidney diseaseKidney diseaseProgressive chronic kidney diseaseDelay kidney failureVariable clinical featuresUric acid levelsControl blood pressureRenal interstitial fibrosisImprove patient outcomesPotential therapeutic targetClinical featuresClinical manifestationsTreatment optionsInterstitial fibrosisInsidious onsetClinical indicationsDisease progressionTubular proteinuriaEarly diagnosisBlood pressurePathological featuresAdvanced stageKidney failureIdentification of plasma proteomic markers underlying polygenic risk of type 2 diabetes and related comorbidities
Loesch D, Garg M, Matelska D, Vitsios D, Jiang X, Ritchie S, Sun B, Runz H, Whelan C, Holman R, Mentz R, Moura F, Wiviott S, Sabatine M, Udler M, Gause-Nilsson I, Petrovski S, Oscarsson J, Nag A, Paul D, Inouye M. Identification of plasma proteomic markers underlying polygenic risk of type 2 diabetes and related comorbidities. Nature Communications 2025, 16: 2124. PMID: 40032831, PMCID: PMC11876343, DOI: 10.1038/s41467-025-56695-z.Peer-Reviewed Original ResearchMeSH KeywordsBiomarkersCardiovascular DiseasesComorbidityDiabetes Mellitus, Type 2Extracellular Matrix ProteinsFemaleGenetic Predisposition to DiseaseGenome-Wide Association StudyHumansInsulin-Like Growth Factor Binding Protein 2MaleMiddle AgedMultifactorial InheritanceProteomicsRisk FactorsUnited KingdomConceptsPolygenic scoresNon-coding variantsEtiology of type 2 diabetesMolecular dataVariant effectsPathway enrichmentPlasma proteomic markersPotential therapeutic targetType 2 diabetesProteinDisease biologyPolygenic riskUK BiobankProteomic markersTherapeutic targetPathwayCirculating proteinsGenomeRisk of type 2 diabetesCardiometabolic scoreBiologyInteractive portalVariantsEnrichmentDiabetes comorbiditiesEndothelial SHANK3 regulates tight junctions in the neonatal mouse blood-brain barrier through β-Catenin signaling
Kim Y, Kim M, Kim S, Lee R, Ujihara Y, Marquez-Wilkins E, Jiang Y, Yang E, Kim H, Lee C, Park C, Kim I. Endothelial SHANK3 regulates tight junctions in the neonatal mouse blood-brain barrier through β-Catenin signaling. Nature Communications 2025, 16: 1407. PMID: 39915488, PMCID: PMC11802743, DOI: 10.1038/s41467-025-56720-1.Peer-Reviewed Original ResearchConceptsBlood-brain barrierNeuronal excitabilityB-cateninBarrier functionMouse blood-brain barrierReduced neuronal excitabilityMale mutant miceBlood-brain barrier permeabilityBrain endothelial cellsAutism spectrum disorderNeonatal micePotential therapeutic targetASD risk genesMutant miceTight junctionsImpaired sociabilityPathogenic mechanismsBrain parenchymaEndothelial cellsTherapeutic targetASD pathogenesisSHANK3Adult ageDisabling conditionMiceChanges in vascular identity during vascular remodeling
Aoyagi Y, Schwartz A, Li Z, Bai H, Gonzalez L, Etchebarne C, Ohashi Y, Kano M, Ho B, Martin K, Dardik A. Changes in vascular identity during vascular remodeling. JVS Vascular Science 2025, 6: 100282. DOI: 10.1016/j.jvssci.2025.100282.Peer-Reviewed Original ResearchArteriovenous fistulaVascular remodelingArterial identityVenous identityVascular identityVascular diseaseCell phenotypeMolecular regulatory pathwaysCellular identityVascular cell phenotypeCellular phenotypesRegulatory pathwaysMolecular markersCOUP-TFIIPotential therapeutic targetPathological vascular remodeling
2024
Comparative proteomic analysis of human vitreous in rhegmatogenous retinal detachment and diabetic retinopathy reveals a common pathway and potential therapeutic target
Brighenti T, Neri G, Mazzola M, Tomé G, Scalfati M, Peroni D, Belli R, Zampedri E, Tebaldi T, Borello U, Romanelli F, Casarosa S. Comparative proteomic analysis of human vitreous in rhegmatogenous retinal detachment and diabetic retinopathy reveals a common pathway and potential therapeutic target. Clinical Proteomics 2024, 21: 63. PMID: 39609746, PMCID: PMC11603643, DOI: 10.1186/s12014-024-09515-3.Peer-Reviewed Original ResearchRhegmatogenous retinal detachmentDiabetic retinopathyNon-steroidal anti-inflammatory drugsRetinal detachmentVitreoretinal diseasesPotential therapeutic targetProliferative vitreoretinopathyOphthalmic non-steroidal anti-inflammatory drugTherapeutic targetAnalysis of vitreous samplesProteomic signatureGlucose metabolismNitric oxide levelsAnti-inflammatory drugsElevated nitric oxide levelsMacular puckerPhotoreceptor deathImprove quality of lifeAldo-keto reductase family 1 member B1Vitreous samplesRetinal cellsVascular proliferationFibrous proliferationReduce complicationsHuman vitreousPilY1 regulates the dynamic architecture of the type IV pilus machine in Pseudomonas aeruginosa
Guo S, Chang Y, Brun Y, Howell P, Burrows L, Liu J. PilY1 regulates the dynamic architecture of the type IV pilus machine in Pseudomonas aeruginosa. Nature Communications 2024, 15: 9382. PMID: 39477930, PMCID: PMC11525922, DOI: 10.1038/s41467-024-53638-y.Peer-Reviewed Original ResearchConceptsPilus extensionCell envelopeType IV piliPathogen Pseudomonas aeruginosaBacterial cell envelopeP. aeruginosa cellsCryo-electron tomographyPilus dynamicsPilin subunitSecretin channelSurface motilityPriming complexOuter membraneBiofilm formationT4PPilY1P. aeruginosaPseudomonas aeruginosaCentral poreMolecular mechanismsSubtomogram averagingPotential therapeutic targetDynamic assemblyTherapeutic targetMolecular frameworkThe role of parvalbumin interneuron dysfunction across neurodegenerative dementias
Smeralda C, Pandit S, Turrini S, Reilly J, Palmisano A, Sprugnoli G, Hampel H, Benussi A, Borroni B, Press D, Rotenberg A, El Fakhri G, Koch G, Rossi S, Santarnecchi E. The role of parvalbumin interneuron dysfunction across neurodegenerative dementias. Ageing Research Reviews 2024, 101: 102509. PMID: 39306248, DOI: 10.1016/j.arr.2024.102509.Peer-Reviewed Original ResearchInterneuron dysfunctionCortical hyperexcitabilityTherapeutic targetCortical excitation/inhibition balanceRhythm disruptionFast-spikingPV+ cellsBasket neuronsPotential therapeutic targetInhibitory interneuronsExcitation/inhibition balanceOscillatory disruptionsSymptom onsetNovel biomarkersHyperexcitabilityDysfunctionNeuronal deathOscillatory activityDementia with Lewy bodiesPathophysiological frameworkClinical symptom onsetFrontotemporal dementiaAldehydes alter TGF-β signaling and induce obesity and cancer
Yang X, Bhowmick K, Rao S, Xiang X, Ohshiro K, Amdur R, Hassan M, Mohammad T, Crandall K, Cifani P, Shetty K, Lyons S, Merrill J, Vegesna A, John S, Latham P, Crawford J, Mishra B, Dasarathy S, Wang X, Yu H, Wang Z, Huang H, Krainer A, Mishra L. Aldehydes alter TGF-β signaling and induce obesity and cancer. Cell Reports 2024, 43: 114676. PMID: 39217614, PMCID: PMC11560041, DOI: 10.1016/j.celrep.2024.114676.Peer-Reviewed Original ResearchAldehyde dehydrogenase 2Small interfering RNADisease progression to cancerPro-oncogenic phenotypeTGF-bProgression to cancerGrowth factor BTGF-b signalingHuman metabolic syndromeSteatotic liver diseasePotential therapeutic targetMetabolic syndromePro-fibroticInduce obesityTherapeutic inhibitionLiver diseaseCurrent treatmentSmad3 signalingGlucose handlingTherapeutic targetFunctional phenotypeDehydrogenase 2Improve glucose handlingSPTBN1ObesityIntestinal Nogo-B reduces GLP1 levels by binding to proglucagon on the endoplasmic reticulum to inhibit PCSK1 cleavage
Gong K, Xue C, Feng Z, Pan R, Wang M, Chen S, Chen Y, Guan Y, Dai L, Zhang S, Jiang L, Li L, Wang B, Yin Z, Ma L, Iwakiri Y, Tang J, Liao C, Chen H, Duan Y. Intestinal Nogo-B reduces GLP1 levels by binding to proglucagon on the endoplasmic reticulum to inhibit PCSK1 cleavage. Nature Communications 2024, 15: 6845. PMID: 39122737, PMCID: PMC11315690, DOI: 10.1038/s41467-024-51352-3.Peer-Reviewed Original ResearchConceptsEnteroendocrine cellsEndoplasmic reticulum (ER)-resident proteinGlucagon-like peptide 1Nogo-BEndoplasmic reticulumStimulate insulin secretionPotential therapeutic targetProglucagonGlucagon-like peptide 1 receptorInhibit glucagon secretionRegulatory processesIntestinal tractProglucagon fragmentInsulin secretionCleavageNogo-B knockoutTherapeutic targetPancreatic cellsPeptide 1Glucagon secretionCellsReticulonGolgiReticulon 4BInsulin resistanceTIGIT expression in renal cell carcinoma infiltrating T cells is variable and inversely correlated with PD-1 and LAG3
Perales O, Jilaveanu L, Adeniran A, Su D, Hurwitz M, Braun D, Kluger H, Schoenfeld D. TIGIT expression in renal cell carcinoma infiltrating T cells is variable and inversely correlated with PD-1 and LAG3. Cancer Immunology, Immunotherapy 2024, 73: 192. PMID: 39105820, PMCID: PMC11303630, DOI: 10.1007/s00262-024-03773-8.Peer-Reviewed Original ResearchConceptsRenal cell carcinomaRenal cell carcinoma tumorsT cellsTIGIT expressionCheckpoint inhibitorsPD-1Likelihood of response to therapyTumor-infiltrating T cellsCD3+ T cellsRenal cell carcinoma metastasisTreatment of renal cell carcinomaImmune checkpoint inhibitorsInfiltrating T cellsPurposeImmune checkpoint inhibitorsResponse to therapyT cell immunoglobulinCD3+ levelsMetastatic RCC specimensAdjacent normal renal tissuesNormal renal tissuesQuantitative immunofluorescence analysisCell carcinomaResistant diseasePotential therapeutic targetTissue microarrayClonal cytopenia of undetermined significance: definitions, risk and therapeutic targets
Taborda C, Zeidan A, Mendez L. Clonal cytopenia of undetermined significance: definitions, risk and therapeutic targets. Frontiers In Hematology 2024, 3: 1419323. DOI: 10.3389/frhem.2024.1419323.Peer-Reviewed Original ResearchClonal hematopoiesis of indeterminate potentialClonal hematopoiesisClonal cytopeniaSomatic genetic alterationsTherapeutic targetStem/progenitor cell populationsRisk stratification toolBlood of individualsMyeloid malignanciesMyeloid neoplasmsHematologic malignanciesPotential therapeutic targetIndeterminate potentialRisk stratificationBlood countGenetic alterationsStratification toolClinical investigationNatural historyCell populationsCytopeniasMalignancyBloodRiskCytopenia(sCurrent understanding and new insights in the treatment of IgA nephropathy
Zhang Y, Zhang H. Current understanding and new insights in the treatment of IgA nephropathy. Nephrology 2024, 29: 75-79. PMID: 38958055, DOI: 10.1111/nep.14340.Peer-Reviewed Original ResearchIgA nephropathyProgression to end-stage kidney diseaseRisk of progression to end-stage kidney diseaseTreatment of IgA nephropathyEra of targeted treatmentCurrent treatment strategiesEnd-stage kidney diseaseDownstream complement activationDevelopment of IgANRandomized controlled trialsImmunosuppressive approachesPotential therapeutic targetPrimary glomerulonephritisKDIGO guidelinesOff-labelTreatment strategiesKidney diseaseIgANPathogenic mechanismsControlled trialsTreatment approachesComplement activationDisease pathogenesisTherapeutic targetNephropathyGlycolysis in hepatic stellate cells coordinates fibrogenic extracellular vesicle release spatially to amplify liver fibrosis
Khanal S, Liu Y, Bamidele A, Wixom A, Washington A, Jalan-Sakrikar N, Cooper S, Vuckovic I, Zhang S, Zhong J, Johnson K, Charlesworth M, Kim I, Yeon Y, Yoon S, Noh Y, Meroueh C, Timbilla A, Yaqoob U, Gao J, Kim Y, Lucien F, Huebert R, Hay N, Simons M, Shah V, Kostallari E. Glycolysis in hepatic stellate cells coordinates fibrogenic extracellular vesicle release spatially to amplify liver fibrosis. Science Advances 2024, 10: eadn5228. PMID: 38941469, PMCID: PMC11212729, DOI: 10.1126/sciadv.adn5228.Peer-Reviewed Original ResearchConceptsHepatic stellate cellsLiver fibrosisExtracellular vesiclesEV releaseHistone 3 lysine 9 acetylationExtracellular vesicle releaseIncreased EV releaseFibrotic gene expressionNanosized extracellular vesiclesPromoter regionVesicle releasePotential therapeutic targetGene expressionGenetic inhibitionSpatial transcriptomicsStellate cellsGlycolysisUp-regulatedFibrosisTherapeutic targetPericentral zoneLiverPathwayAmplificationExpressionEffect of CDC7 inhibition and MYC degradation on neuroendocrine transformation in the lung and prostate cancer.
Quintanal-Villalonga A, Kawasaki K, Redin E, Rakhade S, Durani V, Sabet A, Karthaus W, Zaidi S, Zhan Y, Manoj P, Sridhar H, Zhong H, Mello B, Ciampricotti M, Bhanot U, Haffner M, Socci N, Yu H, Chan J, Rudin C. Effect of CDC7 inhibition and MYC degradation on neuroendocrine transformation in the lung and prostate cancer. Journal Of Clinical Oncology 2024, 42: e20105-e20105. DOI: 10.1200/jco.2024.42.16_suppl.e20105.Peer-Reviewed Original ResearchRisk of transformationNE transformationProstatic adenocarcinomaTherapeutic vulnerabilitiesMYC degradationPhase II clinical trialLung tumor modelDelays tumor relapseII clinical trialsTherapy in vivoIn vivo prostateMechanisms of resistanceMYC isoformsNE phenotypeTumor relapseUntreated tumorsNeuroendocrine transformationProstate cancerStemness transcription factorsPotential therapeutic targetTargeted therapyPoor prognosisTumor modelProstateTumor populationGlis2 is an early effector of polycystin signaling and a target for therapy in polycystic kidney disease
Zhang C, Rehman M, Tian X, Pei S, Gu J, Bell T, Dong K, Tham M, Cai Y, Wei Z, Behrens F, Jetten A, Zhao H, Lek M, Somlo S. Glis2 is an early effector of polycystin signaling and a target for therapy in polycystic kidney disease. Nature Communications 2024, 15: 3698. PMID: 38693102, PMCID: PMC11063051, DOI: 10.1038/s41467-024-48025-6.Peer-Reviewed Original ResearchConceptsMouse models of autosomal dominant polycystic kidney diseaseModel of autosomal dominant polycystic kidney diseasePolycystin signalingAutosomal dominant polycystic kidney diseasePolycystin-1Polycystic kidney diseaseTreat autosomal dominant polycystic kidney diseaseGlis2Primary ciliaKidney tubule cellsSignaling pathwayMouse modelDominant polycystic kidney diseasePotential therapeutic targetTranslatomeAntisense oligonucleotidesKidney diseasePolycystinMouse kidneyFunctional effectorsCyst formationTherapeutic targetInactivationFunctional targetPharmacological targetsTherapeutic Targeting of DNA Repair Pathways in Pediatric Extracranial Solid Tumors: Current State and Implications for Immunotherapy
Zhao S, Prior D, Heske C, Vasquez J. Therapeutic Targeting of DNA Repair Pathways in Pediatric Extracranial Solid Tumors: Current State and Implications for Immunotherapy. Cancers 2024, 16: 1648. PMID: 38730598, PMCID: PMC11083679, DOI: 10.3390/cancers16091648.Peer-Reviewed Original ResearchDNA damage repair inhibitorsPediatric extracranial solid tumorDNA damage repair deficiencyExtracranial solid tumorSolid tumorsDNA damage repairResponse to immune checkpoint blockadeCombinations of DDR inhibitorsEnhance tumor immunogenicityImmune checkpoint blockadePediatric solid tumorsTherapeutic targetPediatric clinical trialsDNA damage repair pathwaysDDR pathwaysCheckpoint blockadeTumor immunogenicityDNA damagePediatric tumorsPotential therapeutic targetDDR inhibitorsClinical trialsTumorHuman cancersRepair DNA damageThe 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 degradationSecretionCellsMuscleTWEAKAn evolutionarily conserved ubiquitin ligase drives infection and transmission of flaviviruses
Wu L, Zhang L, Feng S, Chen L, Lin C, Wang G, Zhu Y, Wang P, Cheng G. An evolutionarily conserved ubiquitin ligase drives infection and transmission of flaviviruses. Proceedings Of The National Academy Of Sciences Of The United States Of America 2024, 121: e2317978121. PMID: 38593069, PMCID: PMC11032495, DOI: 10.1073/pnas.2317978121.Peer-Reviewed Original ResearchConceptsNonstructural proteinsSingle-stranded RNA genomeER-associated degradationE3 ligase HRD1Individual functional proteinsFlavivirus infectionCellular fitnessRNA genomeUbiquitin systemFlavivirus NS4AFunctional proteinsFlavivirus proteinsLysine residuesMammalian hostsMosquito-borne flavivirusSmall molecule inhibitorsStructural proteinsHrd1Viral proteinsProgeny virionsUbiquitinPotential therapeutic targetDENV2 infectionProteinNS4AAbstract 2759: Transcriptional intra-tumoral heterogeneity of putative therapeutic targets in colorectal cancer peritoneal metastases
Zhao J, Ong J, Chia D, Teo M, Tan Q, Ng G, Tan J, Ma H, Ong X, Tay S, Tan P, Sundar R. Abstract 2759: Transcriptional intra-tumoral heterogeneity of putative therapeutic targets in colorectal cancer peritoneal metastases. Cancer Research 2024, 84: 2759-2759. DOI: 10.1158/1538-7445.am2024-2759.Peer-Reviewed Original ResearchColorectal cancer peritoneal metastasesCRC PMPeritoneal metastasisColorectal cancerIntra-tumor heterogeneitySystemic regimensTherapeutic targetAmerican Association for Cancer Research annual meetingsPrognosis of peritoneal metastasisResistant to systemic chemotherapyPlasma-peritoneal barrierOncological surgical resectionColorectal cancer patientsSystemic chemotherapySurgical resectionPalliative surgerySystemic therapyAntineoplastic therapyPotential therapeutic targetExploratory laparotomyTranscoelomic metastasisPoor prognosisFFPE tissue samplesSynchronous PMPoor responseTransmembrane pH gradient imaging in rodent glioma models
Mishra S, Santana J, Mihailovic J, Hyder F, Coman D. Transmembrane pH gradient imaging in rodent glioma models. NMR In Biomedicine 2024, 37: e5102. PMID: 38263680, PMCID: PMC10987279, DOI: 10.1002/nbm.5102.Peer-Reviewed Original ResearchNormal tissuesRodent glioma modelsGL261 gliomasU87 gliomasTumor microenvironmentPotential therapeutic targetGlioma modelTumor survivalExtracellular acidosisTumorMetabolic reprogrammingRegulate drug deliveryIntracellular pHRat brainExtracellular pHTherapeutic targetGliomaMouse brainDrug deliveryIntracellular milieuTransmembrane pH gradientBrainSubmillimeter resolutionTissueCells
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