Wenyi Luo, MD, PhD
he/him/his
Assistant Professor of PathologyDownloadHi-Res Photo
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Pathology
Primary
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Pathology
310 Cedar St
New Haven, CT 06510
United States
About
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Assistant Professor of Pathology
Biography
Wenyi Luo, MD, PhD, is an Assistant Professor of Pathology specializing in Anatomic Pathology and GI Pathology. Dr. Luo came to Yale Pathology from the University of Oklahoma Health Sciences Center (OUHSC), where he served as Assistant Professor and General Surgical Pathologist in the Department of Pathology. At OUHSC, he also served as Director of the Immunohistochemistry Lab, Director of Resident Surgical Pathology Rotation, and was a member of the OU Health Stephenson Cancer Center.
Dr. Luo earned a Bachelor of Medicine and a Master of Medicine at Peking University Health Science Center, China, and a PhD in Genetics at the University of Alabama Birmingham (UAB). He served as a Resident at Peking University Health Science Center, was a Postdoctoral Research Fellow at UAB, an AP/CP Resident at OUHSC, and completed a Surgical Pathology Fellowship and a Gastrointestinal Pathology Fellowship, both at MD Anderson Cancer Center in Houston. Dr. Luo is board certified in Anatomic and Clinical Pathology.
Appointments
Pathology
Assistant ProfessorPrimary
Other Departments & Organizations
- Anatomic Pathology
- Pathology
- Yale Medicine
Education & Training
- Surgical Pathology Fellowship
- University of Texas MD Anderson Cancer Center (2023)
- Gastrointestinal and Liver Pathology Fellowship
- University of Texas MD Anderson Cancer Center (2023)
- Anatomic and Clinical Pathology Residency, Chief
- University of Oklahoma Health Sciences Center (2017)
- Postdoctoral Research Fellow
- University of Alabama at Birmingham (2013)
- PhD
- University of Alabama at Birmingham, Genetics (2010)
- MD
- Peking University Health Science Center (2004)
Research
Research at a Glance
Yale Co-Authors
Frequent collaborators of Wenyi Luo's published research.
Publications Timeline
A big-picture view of Wenyi Luo's research output by year.
Shaoning Jiang
44Publications
1,151Citations
Publications
2024
Gly-β-MCA is a potent anti-cholestasis agent against “human-like” hydrophobic bile acid-induced biliary injury in mice
Hasan M, Wang H, Luo W, Clayton Y, Gu L, Du Y, Palle S, Chen J, Li T. Gly-β-MCA is a potent anti-cholestasis agent against “human-like” hydrophobic bile acid-induced biliary injury in mice. Journal Of Lipid Research 2024, 65: 100649. PMID: 39306039, PMCID: PMC11526081, DOI: 10.1016/j.jlr.2024.100649.Peer-Reviewed Original ResearchConceptsUrsodeoxycholic acid treatmentUrsodeoxycholic acidPortal fibrosisHepatobiliary injuryClinically relevant dosesMuricholic acidsChronic liver diseaseBile acidsEndogenous bile acidsHydrophobic bile acidsPortal inflammationBile acid pool compositionLithocholic acidTherapeutic optionsBiliary injuryKO miceLine drugsBile acid pool sizeSerum transaminasesBile acid poolRelevant dosesDuctular reactionLiver diseaseCholestasisCholestasis modelThe 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 ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsPancreatic cancer cachexiaTumor cellsCancer cachexiaTherapeutic targetLimited treatment optionsPancreatic cancer cellsImmune microenvironmentCCL2/CCR2 axisPotential therapeutic targetTreatment optionsMuscle wastingReprogram macrophagesTumorMuscle atrophyCachexiaCancer cellsMacrophagesNon-autonomous activationMuscle remodelingCancerMuscle degradationSecretionCellsMuscleTWEAK
2023
Clinical Features and Management of Acute and Chronic Radiation-Induced Colitis and Proctopathy
Abu-Sbeih H, Tang T, Ali F, Ma W, Shatila M, Luo W, Tan D, Tang C, Richards D, Ge P, Thomas A, Wang Y. Clinical Features and Management of Acute and Chronic Radiation-Induced Colitis and Proctopathy. Cancers 2023, 15: 3160. PMID: 37370770, PMCID: PMC10296205, DOI: 10.3390/cancers15123160.Peer-Reviewed Original ResearchConceptsArgon plasma coagulationRadiation therapyMedical managementAPC treatmentSingle tertiary cancer centerRadiation-induced colitisManagement of AcuteNon-bloody diarrheaRetrospective observational studyTertiary cancer centerCancer patients' qualityLogistic regression analysisClinical characteristicsEndoscopic therapySymptom onsetPredominant symptomClinical featuresEndoscopic characteristicsPatients' qualityCancer CenterClinical variablesBloody diarrheaCancer patientsFemale sexFrequent findingAbsence of either Ripk3 or Mlkl reduces incidence of hepatocellular carcinoma independent of liver fibrosis
Mohammed S, Thadathil N, Ohene-Marfo P, Tran A, Van Der Veldt M, Georgescu C, Oh S, Nicklas E, Wang D, Haritha N, Luo W, Janknecht R, Miller B, Wren J, Freeman W, Deepa S. Absence of either Ripk3 or Mlkl reduces incidence of hepatocellular carcinoma independent of liver fibrosis. Molecular Cancer Research 2023, 21: 933-946. PMID: 37204757, PMCID: PMC10472095, DOI: 10.1158/1541-7786.mcr-22-0820.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsNonalcoholic fatty liver diseaseProgression of NAFLDHepatocellular carcinomaChronic inflammationLiver fibrosisMale miceMouse modelCholine-deficient high-fat dietFemale wild-type miceOncogenic pathwaysFatty liver diseaseMarkers of inflammationHigh-fat dietLow-fat dietDevelopment of inflammationValid therapeutic targetWild-type miceHepatic inflammationInflammation contributesLiver diseaseWT miceFemale miceSex-specific differencesInflammationTherapeutic targetCombining ASBT inhibitor and FGF15 treatments enhances therapeutic efficacy against cholangiopathy in female but not male Cyp2c70 KO mice
Hasan M, Chen J, Matye D, Wang H, Luo W, Gu L, Clayton Y, Du Y, Li T. Combining ASBT inhibitor and FGF15 treatments enhances therapeutic efficacy against cholangiopathy in female but not male Cyp2c70 KO mice. Journal Of Lipid Research 2023, 64: 100340. PMID: 36737039, PMCID: PMC9986646, DOI: 10.1016/j.jlr.2023.100340.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsBile acid poolKO miceTherapeutic efficacyHepatobiliary injuryBile acid pool sizeBile acid exposureGut barrier integrityGut barrier functionBile acid metabolismAcid poolBile acid synthesisAcid pool sizeBile acid uptakePortal inflammationPortal fibrosisGut exposureDuctular reactionGSK2330672Therapeutic reductionUrsodeoxycholic acidMuricholic acidAcid exposureASBT inhibitorSevere cholangiopathyBarrier integrity
2022
17α-estradiol, a lifespan-extending compound, attenuates liver fibrosis by modulating collagen turnover rates in male mice
Ali Mondal S, Sathiaseelan R, Mann S, Kamal M, Luo W, Saccon T, Isola J, Peelor F, Li T, Freeman W, Miller B, Stout M. 17α-estradiol, a lifespan-extending compound, attenuates liver fibrosis by modulating collagen turnover rates in male mice. AJP Endocrinology And Metabolism 2022, 324: e120-e134. PMID: 36516471, PMCID: PMC9902223, DOI: 10.1152/ajpendo.00256.2022.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsLiver fibrosisMale miceCombination hormone replacement therapyMatrix metalloproteinase-2 activityHepatic stellate cell activationChronic liver diseaseHormone replacement therapySubset of womenMetalloproteinase-2 activityStellate cell activationGrowth factor-β1Proinflammatory macrophage activationFibrotic burdenCollagen synthesis ratesChronic treatmentLiver diseaseReplacement therapyCytokine expressionMacrophage contentImmune cellsTGF-β1Estrogen signalingHSC activationFactor-β1Macrophage activationmiR-130b/301b Is a Negative Regulator of Beige Adipogenesis and Energy Metabolism In Vitro and In Vivo.
Luo W, Kim Y, Jensen M, Herlea-Pana O, Wang W, Rudolph M, Friedman J, Chernausek S, Jiang S. miR-130b/301b Is a Negative Regulator of Beige Adipogenesis and Energy Metabolism In Vitro and In Vivo. Diabetes 2022, 71: 2360-2371. PMID: 36001751, PMCID: PMC9630090, DOI: 10.2337/db22-0205.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsBeige adipogenesisMiR-301bMiR-130bPeroxisome proliferator-activated receptor γ coactivator 1αProliferator-activated receptor γ coactivator 1αImproved glucose toleranceReceptor γ coactivator 1αLess weight gainPotential therapeutic targetCold-induced energy expenditureΓ coactivator 1αMitochondrial biogenesisMetabolic complicationsVisceral adiposityGlucose toleranceThermogenic brownCounteract obesityMetabolic disordersTherapeutic targetAdipose tissueBeige phenotypeMetabolic diseasesAdipose progenitor cellsBeige adipocytesCoactivator 1αSenolytic treatment reduces cell senescence and necroptosis in Sod1 knockout mice that is associated with reduced inflammation and hepatocellular carcinoma
Thadathil N, Selvarani R, Mohammed S, Nicklas E, Tran A, Kamal M, Luo W, Brown J, Lawrence M, Borowik A, Miller B, Van Remmen H, Richardson A, Deepa S. Senolytic treatment reduces cell senescence and necroptosis in Sod1 knockout mice that is associated with reduced inflammation and hepatocellular carcinoma. Aging Cell 2022, 21: e13676. PMID: 35869934, PMCID: PMC9381894, DOI: 10.1111/acel.13676.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsSod1KO miceHepatocellular carcinomaQ treatmentCellular senescenceSenescence-associated secretory phenotype factorsMarkers of necroptosisSod1 knockout miceChronic liver diseaseMarkers of inflammationMonths of ageExpression of p16WT levelsSenolytic treatmentLiver diseaseReduced inflammationCu/Zn-superoxide dismutaseMacrophage levelsLiver fibrosisPhenotype factorsLiver cancerNecrostatin-1sKnockout miceAge-associated pathologiesMice nullInflammationAcetyl-Coenzyme A Synthetase 2 Potentiates Macropinocytosis and Muscle Wasting Through Metabolic Reprogramming in Pancreatic Cancer
Zhou Z, Ren Y, Yang J, Liu M, Shi X, Luo W, Fung K, Xu C, Bronze M, Zhang Y, Houchen C, Li M. Acetyl-Coenzyme A Synthetase 2 Potentiates Macropinocytosis and Muscle Wasting Through Metabolic Reprogramming in Pancreatic Cancer. Gastroenterology 2022, 163: 1281-1293.e1. PMID: 35777482, PMCID: PMC9613512, DOI: 10.1053/j.gastro.2022.06.058.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsMetabolic reprogrammingDynamin 2Transcriptional activationShort palindromic repeat-associated protein 9 (CRISPR/Cas9) systemSingle-cell RNA sequencing dataRNA sequencing dataProtein 9 (Cas9) systemGlycogen synthase kinasePancreatic cancerEpigenetic reprogrammingFamily member 2Chromatin immunoprecipitationMuscle wastingDownstream targetsSequencing dataSyndecan-1ReprogrammingSynthase kinaseWorse prognosisMacropinocytosisZIP4ACSS2Mouse modelProtein 4Uptake assaysCalcifying nested stromal-epithelial tumor of the liver with recurrence in a transplanted liver – A clinical report with literature review
Kamal M, Atwi D, Gatalica Z, Luo W. Calcifying nested stromal-epithelial tumor of the liver with recurrence in a transplanted liver – A clinical report with literature review. Human Pathology Reports 2022, 28: 300620. DOI: 10.1016/j.hpr.2022.300620.Peer-Reviewed Original ResearchCitationsConceptsStromal-epithelial tumorAggressive clinical courseSmall blue cellsTERT promoter mutationsRare liver neoplasmLiver transplantationClinical courseFemale predominanceLiver failureTransplanted liverRare tumorRecurrence 3Unknown histogenesisImmunohistochemical spectrumLiver neoplasmsDiffuse positivityClinical reportsTumorsBlue cellsYoung adultsCNSETPromoter mutationsMolecular featuresPIK3CAPathologic mutations
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Pathology
310 Cedar St
New Haven, CT 06510
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