2025
Moderate alcohol-associated hepatitis: A real-world multicenter study
Idalsoaga F, Díaz L, Dunn W, Mehta H, Muñoz K, Caldentey V, Arnold J, Ayares G, Mortuza R, Sarin S, Maiwall R, Zhang W, Qian S, Simonetto D, Singal A, Elfeki M, Ramirez-Cadiz C, Malhi G, Ahmed A, Homsi H, Abid Z, Cabezas J, Echavarría V, Poca M, Soriano G, Cuyas B, Cots M, La Tijera M, Ayala-Valverde M, Perez D, Gomez J, Abraldes J, Al-Karaghouli M, Jalal P, Ibrahim M, García-Tsao G, Goyes D, Skladaný L, Havaj D, Sulejova K, Selcanova S, Rincón D, Chacko K, Restrepo J, Yaquich P, Toro L, Shah V, Arrese M, Kamath P, Bataller R, Arab J. Moderate alcohol-associated hepatitis: A real-world multicenter study. Hepatology Communications 2025, 9: e0673. PMID: 40131003, PMCID: PMC11936654, DOI: 10.1097/hc9.0000000000000673.Peer-Reviewed Original ResearchConceptsSevere alcohol-associated hepatitisNeutrophil-to-lymphocyte ratioMaddrey's discriminant functionModerate AHMultiple organ failureOrgan failureMulticenter retrospective cohort studyAlcohol-associated hepatitisCumulative survival rateRetrospective cohort studyReceiver operating characteristic curveLong-term outcomesShort-term mortalityMortality scoring systemsPrognostic factorsSerum bilirubinMELD scoreWell-characterized diseaseClinical profileMedian MELDCohort studyCox regressionMultivariate analysisTherapeutic strategiesSurvival rateThe Molecular Basis of Polycystic Ovary Syndrome and Its Cardiometabolic Correlates: Exploring the Intersection and Its Clinical Implications—A Narrative Review
Mahabamunuge J, Sekula N, Lepore C, Kudrimoti M, Upadhyay A, Alshowaikh K, Li H, Seifer D, AlAshqar A. The Molecular Basis of Polycystic Ovary Syndrome and Its Cardiometabolic Correlates: Exploring the Intersection and Its Clinical Implications—A Narrative Review. Biomedicines 2025, 13: 709. PMID: 40149685, PMCID: PMC11940587, DOI: 10.3390/biomedicines13030709.Peer-Reviewed Original ResearchPolycystic ovary syndromeType 2 diabetes mellitusCardiometabolic morbidityIncreased cardiovascular riskDevelopment of hypertensionCardiovascular risk factorsNarrative reviewPotential clinical implicationsAndrogen excessEndothelial dysfunctionCardiovascular riskClinical conditionsPredisposed individualsTherapeutic strategiesAdipokine secretionRisk factorsInsulin resistanceCardiometabolic diseasesCardiovascular diseaseClinical implicationsMorbidityMellitusSyndromeMolecular mechanismsDiseasePrecision projections of the delay of resistance mutations in non-small cell lung cancer via suppression of APOBEC
Nousias O, Mandell J, Anderson K, Townsend J. Precision projections of the delay of resistance mutations in non-small cell lung cancer via suppression of APOBEC. Lung Cancer 2025, 202: 108487. PMID: 40090261, DOI: 10.1016/j.lungcan.2025.108487.Peer-Reviewed Original ResearchNon-small cell lung cancer patientsNon-small cell lung cancerCell lung cancer patientsCell lung cancerLung cancer patientsEvolution of drug resistanceLung cancerDrug resistanceCancer patientsTyrosine kinase inhibitor therapyKinase inhibitor therapyTyrosine kinase inhibitorsPersonalized therapeutic strategiesTKI therapyInhibitor therapyTherapeutic failureResistance mutationsTherapeutic efficacyKinase inhibitorsAPOBEC mutationsTherapeutic strategiesTreatment efficacyCancer progressionImprove outcomesCancerCardiac Magnetic Resonance Imaging in Immune Checkpoint Inhibitor–Related Myocarditis
Hammer M, Tysarowski M, Fuss C, Bader A. Cardiac Magnetic Resonance Imaging in Immune Checkpoint Inhibitor–Related Myocarditis. Echocardiography 2025, 42: e70131. PMID: 40067334, DOI: 10.1111/echo.70131.Peer-Reviewed Original ResearchConceptsImmune-related adverse eventsImmune checkpoint inhibitorsCardiac magnetic resonance imagingMagnetic resonance imagingAssociated with immune-related adverse eventsCardiac immune-related adverse eventsMechanisms of immune checkpoint inhibitorsICI-associated myocarditisICI-related myocarditisResonance imagingPersonalized cancer immunotherapySevere cardiovascular complicationsImmune tolerance pathwayCheckpoint inhibitorsCancer immunotherapyCardiac complicationsCombination therapyTumor cytotoxicityClinical presentationCardiovascular complicationsAdverse eventsTherapeutic efficacyOncological treatmentTherapeutic strategiesMyocarditisAn 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 phagocytosisSuppression of endothelial ceramide de novo biosynthesis by Nogo-B contributes to cardiometabolic diseases
Rubinelli L, Manzo O, Sungho J, Del Gaudio I, Bareja R, Marino A, Palikhe S, Di Mauro V, Bucci M, Falcone D, Elemento O, Ersoy B, Diano S, Sasset L, Di Lorenzo A. Suppression of endothelial ceramide de novo biosynthesis by Nogo-B contributes to cardiometabolic diseases. Nature Communications 2025, 16: 1968. PMID: 40000621, PMCID: PMC11862206, DOI: 10.1038/s41467-025-56869-9.Peer-Reviewed Original ResearchConceptsNogo-BEndothelial dysfunctionHFD miceCardiometabolic diseasesSphingolipid signalingDevelopment of therapeutic strategiesBioactive sphingolipidsCeramide degradationSphingosine-1-phosphateHepatic glucose productionIn vivo evidenceEndothelial cellsEndothelial specific deletionCeramideBiosynthesisHigh-fat dietPathological implicationsSphingolipidsGlucose productionHFDIn vivoMale miceMetabolic dysfunctionTherapeutic strategiesMetabolic disordersAdvancements in the Diagnosis, Treatment, and Risk Stratification of Non-Muscle Invasive Bladder Cancer
Smani S, DuBois J, Zhao K, Sutherland R, Rahman S, Humphrey P, Hesse D, Tan W, Martin D, Lokeshwar S, Ghali F. Advancements in the Diagnosis, Treatment, and Risk Stratification of Non-Muscle Invasive Bladder Cancer. Current Oncology Reports 2025, 1-11. PMID: 39976835, DOI: 10.1007/s11912-025-01645-7.Peer-Reviewed Original ResearchNon-muscle invasive bladder cancerInvasive bladder cancerBladder cancerRisk stratificationBCG-unresponsive NMIBCEarly radical cystectomyTERT promoter mutationsHigh-risk casesLong-term outcomesNadofaragene firadenovecIntravesical therapyTransurethral resectionRadical cystectomyTreatment paradigmStratified careReduce overtreatmentProgression riskIntegration of biomarkersPromoter mutationsClinical trialsTherapeutic strategiesReviewThis reviewPersonalized treatmentAdverse effectsClinical careEffect of Elexacaftor/Tezacaftor/Ivacaftor on Glucose Tolerance in Adolescents With Cystic Fibrosis
Galderisi A, Weiss L, Besançon A, Stremler N, Reix P, Wizla N, Lustre A, Rames C, Tatopoulos A, Perisson C, Dalphin M, Troussier F, Houdouin V, Bessaci K, Cosson L, Gabsi A, Corvol H, Deneuville E, Storni V, Ramel S, Bui S, Heraud M, Remus N, Huet F, Scalbert M, Mely L, Gachelin E, Giannantonio M, Letierce A, Sahki D, Marguet C, Bonnel A, Sermet-Gaudelus I. Effect of Elexacaftor/Tezacaftor/Ivacaftor on Glucose Tolerance in Adolescents With Cystic Fibrosis. The Journal Of Clinical Endocrinology & Metabolism 2025, dgaf099. PMID: 39977216, DOI: 10.1210/clinem/dgaf099.Peer-Reviewed Original ResearchOral glucose tolerance testBaseline oral glucose tolerance testAbnormal glucose toleranceNormal glucose toleranceAbnormal glucose tolerance groupCystic fibrosisGlucose toleranceNormal glucose tolerance groupEffective CFTR modulatorsCF-related diabetesInsulin secretionImpaired fasting glucoseGlucose tolerance testImpaired glucose toleranceForced expiratory volumeBMIz-scoreCFTR modulatorsBaseline characteristicsRelated diabetesFasting glucoseTolerance testTherapeutic strategiesInsulin treatmentExpiratory volumeGlucose levelsLipogenic enzyme FASN promotes mutant p53 accumulation and gain-of-function through palmitoylation
Liu J, Shen Y, Liu J, Xu D, Chang C, Wang J, Zhou J, Haffty B, Zhang L, Bargonetti J, De S, Hu W, Feng Z. Lipogenic enzyme FASN promotes mutant p53 accumulation and gain-of-function through palmitoylation. Nature Communications 2025, 16: 1762. PMID: 39971971, PMCID: PMC11839913, DOI: 10.1038/s41467-025-57099-9.Peer-Reviewed Original ResearchConceptsGain-of-functionTumor suppressive function of p53Mutp53 accumulationAccumulate to high levelsFunction of p53Mutant p53 accumulationTumor suppressive functionMutant p53Subcutaneous xenograft tumor modelMutp53Promote tumorigenesisP53 accumulationPalmitoylationPotential therapeutic strategyXenograft tumor modelFASNTumor modelTumor organoidsTransgenic miceTherapeutic strategiesP53PGLYRP2 drives hepatocyte-intrinsic innate immunity by trapping and clearing hepatitis B virus
Li Y, Ma H, Zhang Y, He T, Li B, Ren H, Feng J, Sheng J, Li K, Qian Y, Wang Y, Zhao H, He J, Li H, Wu H, Yao Y, Shi M. PGLYRP2 drives hepatocyte-intrinsic innate immunity by trapping and clearing hepatitis B virus. Journal Of Clinical Investigation 2025 PMID: 39946201, DOI: 10.1172/jci188083.Peer-Reviewed Original ResearchHepatitis B virusHBV clearanceSpontaneous clearance of hepatitis B virusB virusClear hepatitis B virusClearance of hepatitis B virusHepatitis B virus infectionSpontaneous HBV clearanceAnti-HBV treatmentDNA-binding domainInhibit HBV replicationCovalently closed circular DNAPattern recognition receptorsPotential therapeutic strategyFunctional cureSpontaneous clearanceHost-virus interactionsAge-dependent expressionPathogenic variantsPGRP domainHBV replicationTherapeutic strategiesRecognition receptorsNucleocytoplasmic translocationPGLYRP2Exploring Calcium Channels as Potential Therapeutic Targets in Blast Traumatic Brain Injury
Wachtler N, O’Brien R, Ehrlich B, McGuone D. Exploring Calcium Channels as Potential Therapeutic Targets in Blast Traumatic Brain Injury. Pharmaceuticals 2025, 18: 223. PMID: 40006037, PMCID: PMC11859800, DOI: 10.3390/ph18020223.Peer-Reviewed Original ResearchCalcium signalingCalcium channelsTherapeutic strategiesCalcium homeostasisFunction of calcium channelsDysregulated calcium signalingModulation of injuryTraumatic brain injuryBrain injuryLoss of calcium homeostasisBlast-related traumatic brain injuryDevelopment of neuroprotective interventionsIntracellular calcium dynamicsPlasma membrane stabilityExtracellular calciumBlast traumatic brain injuryPreclinical modelsTherapeutic outcomesNeuroprotective interventionsMembrane abnormalitiesPharmacological inhibitorsNeuronal somataExclusion criteriaCalcium dynamicsSecondary injuryCCL21-CCR7 blockade prevents neuroinflammation and degeneration in Parkinson’s disease models
Leser F, Júnyor F, Pagnoncelli I, Delgado A, Medeiros I, Nóbrega A, Andrade B, de Lima M, da Silva N, Jacob L, Boyé K, Geraldo L, de Souza A, Maron-Gutierrez T, Castro-Faria-Neto H, Follmer C, Braga C, Neves G, Eichmann A, Romão L, Lima F. CCL21-CCR7 blockade prevents neuroinflammation and degeneration in Parkinson’s disease models. Journal Of Neuroinflammation 2025, 22: 31. PMID: 39894839, PMCID: PMC11789347, DOI: 10.1186/s12974-024-03318-x.Peer-Reviewed Original ResearchConceptsMouse model of PDModel of PDMouse modelDopaminergic neuronsNeuron-microglia communicationNeuron-glia communicationParkinson's diseaseCCR7-dependent mannerMicroglial cell activationCCR7 expressionCCL21-CCR7Progressive degenerative diseaseCCR7 receptorMicroglial cell migrationInflammatory profileChemokine CCL21Cell activationCCL21Therapeutic strategiesChemokine inhibitorsTherapeutic implicationsMicroglial activationReceptor pathwayCCR7Behavioral deficitsThe fungal microbiota modulate neonatal oxygen-induced lung injury
Martin I, Silverberg M, Abdelgawad A, Tanaka K, Halloran B, Nicola T, Myers E, Desai J, White C, Karabayir I, Akbilgic O, Tipton L, Gentle S, Ambalavanan N, Peters B, Vu L, Jain V, Lal C, Cormier S, Pierre J, Jilling T, Talati A, Willis K. The fungal microbiota modulate neonatal oxygen-induced lung injury. Microbiome 2025, 13: 24. PMID: 39871397, PMCID: PMC11773857, DOI: 10.1186/s40168-025-02032-x.Peer-Reviewed Original ResearchConceptsBronchopulmonary dysplasiaLung injury severityLung injuryDevelopment of bronchopulmonary dysplasiaSeverity of lung injuryAugmented lung injuryMorbidities of prematurityVery preterm infantsOxygen-induced lung injuryChronic lung diseaseIntestinal microbiomeMicrobiome of infantsPotential therapeutic strategyPreterm infantsNeonatal microbiomePremature infantsPremature neonatesInjury severityMurine modelNeonatal healthLung diseaseMouse modelTherapeutic strategiesLoss of function approachesFungal communitiesHarnessing the tumor microenvironment: targeted cancer therapies through modulation of epithelial-mesenchymal transition
Glaviano A, Lau H, Carter L, Lee E, Lam H, Okina E, Tan D, Tan W, Ang H, Carbone D, Yee M, Shanmugam M, Huang X, Sethi G, Tan T, Lim L, Huang R, Ungefroren H, Giovannetti E, Tang D, Bruno T, Luo P, Andersen M, Qian B, Ishihara J, Radisky D, Elias S, Yadav S, Kim M, Robert C, Diana P, Schalper K, Shi T, Merghoub T, Krebs S, Kusumbe A, Davids M, Brown J, Kumar A. Harnessing the tumor microenvironment: targeted cancer therapies through modulation of epithelial-mesenchymal transition. Journal Of Hematology & Oncology 2025, 18: 6. PMID: 39806516, PMCID: PMC11733683, DOI: 10.1186/s13045-024-01634-6.Peer-Reviewed Original ResearchConceptsEpithelial-mesenchymal transitionTumor microenvironmentCancer progressionTherapeutic resistanceCancer therapyTumor microenvironment componentsTumor microenvironment modulationModulation of epithelial-mesenchymal transitionPromote tumor growthImprove treatment efficacyTumor microenvironment signalsTargeted cancer therapyTarget various componentsTherapeutic challengeTreatment responseTumor growthPromote metastasisTherapeutic strategiesTreatment efficacyEpithelial cellsMesenchymal traitsCancer cellsExtracellular matrix componentsCancerResistance mechanismsChapter 14 Molecular biology, genetic, and epigenetics of kidney tumor
Kazemi R, Rezaeian A, Deyhimfar R, Taheri D. Chapter 14 Molecular biology, genetic, and epigenetics of kidney tumor. 2025, 209-221. DOI: 10.1016/b978-0-443-27302-5.00003-6.Peer-Reviewed Original ResearchDNA damage repair genesKidney cancer developmentRenal cell carcinomaTumor suppressor genePlanning therapeutic strategiesRenal tumorsUrothelial carcinomaWilms tumorCell carcinomaRenal sarcomaKidney tumorsClinical manifestationsUrological cancersKidney cancerPredisposing genesSuppressor geneTherapeutic strategiesCancer developmentTumorRepair genesCancerCarcinomaKidneyGenetic basisGenetic changesChapter 52 Obsessive–compulsive disorder
Abdallah S, Olfson E, Fernandez T. Chapter 52 Obsessive–compulsive disorder. 2025, 937-950. DOI: 10.1016/b978-0-443-19176-3.00011-x.ChaptersObsessive-compulsive disorderObsessive-compulsive disorder etiologiesCognitive behavioral therapySerotonin reuptake inhibitorsReuptake inhibitorsBehavioral therapyMedication augmentationNeuroanatomical alterationsNeurochemical imbalanceMedication trialsGenetic influencesImprove treatment outcomesEvidence-based therapeutic strategiesTreatment outcomesRobust clinical trialsDisordersClinical manifestationsTreatment optionsClinical trialsTherapeutic strategiesSerotoninMultifactorial naturePharmacotherapyNeuromodulationTrialsPhenotypic variability in phosphate transport disorders highlights need for individualized treatment strategies
Zhu Z, Bergwitz C. Phenotypic variability in phosphate transport disorders highlights need for individualized treatment strategies. Kidney International 2025, 107: 12-15. PMID: 39746740, DOI: 10.1016/j.kint.2024.10.020.Peer-Reviewed Original ResearchConceptsPhosphate-wasting disordersIndividualized treatment strategiesLong-term outcomesGenetic variantsPathogenic variantsPhenotypic variabilitySLC34A3 geneClinical presentationTreatment strategiesTreatment challengesTransport disordersTreatment outcomesAffected individualsTherapeutic strategiesPotential treatment challengesBiochemical profileVariantsDisordersGenesOutcomesPhenotypeNpt2cSLC34A3Npt2aThe evolving understanding of systemic mechanisms in organ-specific IgA nephropathy: a focus on gut-kidney crosstalk
Wang X, Zhou X, Qiao X, Falchi M, Liu J, Zhang H. The evolving understanding of systemic mechanisms in organ-specific IgA nephropathy: a focus on gut-kidney crosstalk. Theranostics 2025, 15: 656-681. PMID: 39744688, PMCID: PMC11671385, DOI: 10.7150/thno.104631.Peer-Reviewed Original ResearchConceptsGut-kidney crosstalkExploration of gut microbiotaGut microbiotaKidney diseaseMechanism of IgANIntestinal microbiomeSignaling pathwayIgA nephropathyInter-organ crosstalkEfficient therapeutic strategiesPrognosis of patientsProgression of IgANElaborate mechanismsTherapeutic strategiesIgAN pathogenesisIgANCrosstalkMicrobiomeMicrobiotaMultiple organsKidneyProbioticsNephropathyDiseaseMechanismAdaptations of neutrophils in cancer
Ng M, Cerezo-Wallis D, Ng L, Hidalgo A. Adaptations of neutrophils in cancer. Immunity 2025, 58: 40-58. PMID: 39813993, DOI: 10.1016/j.immuni.2024.12.009.Peer-Reviewed Original Research
2024
OMICS Sciences for Aging Studies
Gómez-Verjan J, Rincón-Heredia R, Poot-Hernández A, Martínez-Magaña J, Montalvo-Ortiz J, Estrella-Parra E, Castillo-Vázquez S, Gutiérrez-Robledo L, Rivero-Segura N. OMICS Sciences for Aging Studies. 2024, 227-237. DOI: 10.1007/978-3-031-76469-1_16.Peer-Reviewed Original Research
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