Ying Chen, MD, PhD
Associate Professor of Epidemiology (Environmental Health)DownloadHi-Res Photo
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Environmental Health Sciences
60 College St, LEPH 521
New Haven, CT 06520
United States
About
Titles
Associate Professor of Epidemiology (Environmental Health)
Biography
Dr. Chen has a broad background in environmental genetics and molecular toxicology, with specific training and expertise in redox biology, oxidative stress related diseases, and transgenic mouse models of redox dysregulation. Her research over the past ten years utilizes unique animal models and applies the system biology approach integrating multi-omics data and histopathology to understand the mechanistic roles of redox homeostasis in disease conditions related to environmental and dietary exposures.
- How does redox-elicited modifications of the liver proteome tune cellular response to protect against alcohol-associated fatty liver disease?
- Does oxidative stress play a mutagenic role in emerging water contaminant 1,4-dioxane-induced liver cancer
- What is the functional crosstalk between antioxidants in the central nervous system as they relate to neuronal health and disease?
- What is the translational importance of these new knowledge in risk assessment, disease prevention and treatment?
Last Updated on February 19, 2023.
Appointments
Environmental Health Sciences
Associate Professor on TermPrimaryEnvironmental Health Sciences
LecturerSecondary
Other Departments & Organizations
Education & Training
- Postdoctoral Research Associate
- University of Colorado (2010)
- Postdoctoral fellow
- University of Cincinnati (2008)
- PhD
- University of Cincinnati, Department of Environmental and Public Health Sciences (2007)
- MD
- Xiangya School of Medicine, Clinical Medicine (1994)
Research
Overview
Dr. Chen’s research focuses on understanding the mechanistic functions of redox homeostasis and antioxidant deficiencies in human diseases associated with environmental and dietary stress. Reduced GSH is the most abundant thiol antioxidant that combats excessive oxidants generated during cellular metabolism or in response to environmental assaults. GSH deficiency has been associated with numerous pathological conditions in human. Dr. Chen’s research work involves the use of unique redox animal models and system biology approach to elucidate the molecular mechanisms underlying liver diseases and neurological disorders.
Specific research projects include:
- Redox-mediated mechanisms in protection against alcohol-associated fatty liver disease
- The mechanistic role of oxidative stress in water contaminant 1,4-dioxane-induced liver cytotoxicity and genotoxicity
- The functional interplay between two antioxidants (glutathione and ascorbate) in the central nervous system
Medical Research Interests
Digestive System Diseases; Disorders of Environmental Origin; Nervous System Diseases; Nutritional and Metabolic Diseases
Public Health Interests
Cancer; Environmental Health; Genetics, Genomics, Epigenetics; Metabolomics
ORCID
0000-0003-4946-4693
Research at a Glance
Yale Co-Authors
Frequent collaborators of Ying Chen's published research.
Publications Timeline
A big-picture view of Ying Chen's research output by year.
David Thompson
Georgia Charkoftaki, PharmD, PhD
Emily Davidson
Rolando Garcia Milian, MLS, AHIP
Jaya Prakash Golla, PhD
Vasilis Vasiliou, PhD
81Publications
5,701Citations
Publications
2025
Gene-dose effect of the glutathione biosynthesis gene on ascorbate deficiency in mice
Strand R, Orlicky D, Chen Y. Gene-dose effect of the glutathione biosynthesis gene on ascorbate deficiency in mice. Biochemical And Biophysical Research Communications 2025, 766: 151900. PMID: 40294460, PMCID: PMC12058385, DOI: 10.1016/j.bbrc.2025.151900.Peer-Reviewed Original ResearchMeSH Keywords and ConceptsConceptsGene-dose effectAscorbate deficiencyTissue GSH levelsDouble-knockoutVitamin CDietary vitamin CAllele dosage effectGlutamate-cysteine ligaseMiceClinical interplayGSH levelsOxidative stressBrain tissueRedox imbalanceGCLMDosage effectBrain functionDeficiencyGlutathione biosynthesis genesIncreased vulnerabilityBrainPhenotypic outcomesModifier subunitRedox balanceGSH biosynthesis
2024
CYP2E1 in 1,4-dioxane metabolism and liver toxicity: insights from CYP2E1 knockout mice study
Wang Y, Charkoftaki G, Orlicky D, Davidson E, Aalizadeh R, Sun N, Ginsberg G, Thompson D, Vasiliou V, Chen Y. CYP2E1 in 1,4-dioxane metabolism and liver toxicity: insights from CYP2E1 knockout mice study. Archives Of Toxicology 2024, 98: 3241-3257. PMID: 39192018, PMCID: PMC11500436, DOI: 10.1007/s00204-024-03811-5.Peer-Reviewed Original ResearchCitationsAltmetricConceptsCYP2E1-null miceLiver toxicityDrinking waterOxidative DNA damageLiver carcinogenAbstract1,4-DioxaneDNA damage repair responseImpaired DNA damage repairWater contaminationOxidative stressElevated oxidative stressEnvironmental pollutionKnockout mouse studiesDamage repair responseCYP2E1-nullMale wildtypeWT miceDNA damageDX exposureRisk assessmentRedox dysregulationCYP2E1 inductionLiver oxidative stressHigh dosesMouse studiesGlutathione synthesis in the mouse liver supports lipid abundance through NRF2 repression
Asantewaa G, Tuttle E, Ward N, Kang Y, Kim Y, Kavanagh M, Girnius N, Chen Y, Rodriguez K, Hecht F, Zocchi M, Smorodintsev-Schiller L, Scales T, Taylor K, Alimohammadi F, Duncan R, Sechrist Z, Agostini-Vulaj D, Schafer X, Chang H, Smith Z, O’Connor T, Whelan S, Selfors L, Crowdis J, Gray G, Bronson R, Brenner D, Rufini A, Dirksen R, Hezel A, Huber A, Munger J, Cravatt B, Vasiliou V, Cole C, DeNicola G, Harris I. Glutathione synthesis in the mouse liver supports lipid abundance through NRF2 repression. Nature Communications 2024, 15: 6152. PMID: 39034312, PMCID: PMC11271484, DOI: 10.1038/s41467-024-50454-2.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsGlutamate-cysteine ligase catalytic subunitLipid abundanceLipogenic enzyme expressionAbundance in vivoLipid productionCatalytic subunitRepress Nrf2Transcription factorsNrf2 repressionAdult tissuesSynthesis of GSHEnzyme expressionNon-redundantRedox bufferMouse liverLoss of GSHTriglyceride productionIn vivo modelsAbundanceGlutathione synthesisLiver balanceFat storesOxidative stressLipidDeletionA Th17 cell-intrinsic glutathione/mitochondrial-IL-22 axis protects against intestinal inflammation
Bonetti L, Horkova V, Grusdat M, Longworth J, Guerra L, Kurniawan H, Franchina D, Soriano-Baguet L, Binsfeld C, Verschueren C, Spath S, Ewen A, Koncina E, Gérardy J, Kobayashi T, Dostert C, Farinelle S, Härm J, Fan Y, Chen Y, Harris I, Lang P, Vasiliou V, Waisman A, Letellier E, Becher B, Mittelbronn M, Brenner D. A Th17 cell-intrinsic glutathione/mitochondrial-IL-22 axis protects against intestinal inflammation. Cell Metabolism 2024, 36: 1726-1744.e10. PMID: 38986617, DOI: 10.1016/j.cmet.2024.06.010.Peer-Reviewed Original ResearchCitationsAltmetricConceptsReactive oxygen speciesMitochondrial functionCatalytic subunit of glutamate cysteine ligaseMitochondrial gene expressionDecreased cellular ATPPhosphorylation of 4E-BP1Disrupt mitochondrial functionReduced phosphorylation of 4E-BP1T cell-specific ablationCell's antioxidant mechanismsCell-specific ablationCatalytic subunitIL-22Cellular signalingIntestinal homeostasisIL-22 productionSignificant reactive oxygen speciesSubunit of glutamate cysteine ligaseGene expressionReduced IL-22 productionReduced phosphorylationCellular ATPGut protectionProtein synthesisGlutamate cysteine ligaseRetinol-binding protein 4 as a promising serum biomarker for the diagnosis and prognosis of hepatocellular Carcinoma.
Wan F, Zhu Y, Wu F, Huang X, Chen Y, Zhou Y, Li H, Liang L, Qin L, Wang Q, He M. Retinol-binding protein 4 as a promising serum biomarker for the diagnosis and prognosis of hepatocellular Carcinoma. Transl Oncol 2024, 45: 101979. PMID: 38728873, DOI: 10.1016/j.tranon.2024.101979.Peer-Reviewed Original ResearchLiver epigenomic signature associated with chronic oxidative stress in a mouse model of glutathione deficiency
Hong S, Yu X, Zhu Y, Chen Y. Liver epigenomic signature associated with chronic oxidative stress in a mouse model of glutathione deficiency. Chemico-Biological Interactions 2024, 398: 111093. PMID: 38830566, PMCID: PMC11223951, DOI: 10.1016/j.cbi.2024.111093.Peer-Reviewed Original ResearchCitationsConceptsS-adenosyl methionineGene promoterArray-based DNA methylation profilingPeripheral blood cellsFatty liver diseaseDNA methylation profilesDNA methylation statusMethyl donor S-adenosyl methionineGene promoter regionFunctional enrichment analysisMethylation enrichmentMouse modelOxidative stressLiver epigenomeEpigenomic changesIn vivo interplayMethylation profilesPromoter regionEpigenetic regulationEpigenomic signaturesEpigenetic mechanismsLipid homeostasisBlood cellsEnrichment analysisCellular survival1,4-Dioxane
Stouffer A, Erickson C, Krick M, Chen Y, Ginsberg G, Loch-Caruso R, Jones R, Madrigal J, Thompson D, Vasliou V. 1,4-Dioxane. 2024, 843-849. DOI: 10.1016/b978-0-12-824315-2.00831-9.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsConceptsPersistent environmental contaminationEnvironmental contaminationEnvironmental behaviorEnvironmental releaseChemical intermediatesWater solubilityPotential negative health effectsDioxaneRecent decadesSoilConsumer productsGroundwaterContaminationHealth effectsSolventSolubilityIntermediatesNegative health effectsStabilizerManagementUsesProductsUseToxicityExposure
2023
Multi-omics profiling reveals cellular pathways and functions regulated by ALDH1B1 in colon cancer cells
Wang Y, Popovic Z, Charkoftaki G, Garcia-Milian R, Lam T, Thompson D, Chen Y, Vasiliou V. Multi-omics profiling reveals cellular pathways and functions regulated by ALDH1B1 in colon cancer cells. Chemico-Biological Interactions 2023, 384: 110714. PMID: 37716420, PMCID: PMC10807983, DOI: 10.1016/j.cbi.2023.110714.Peer-Reviewed Original ResearchCitationsConceptsColon cancer cellsCellular stress response pathwaysStress response pathwaysMulti-omics analysisCancer cellsSecond messenger signalingMulti-omics profilingNew molecular informationFunctional annotationCellular functionsResponse pathwaysKinase signalingCellular pathwaysColon adenocarcinoma cell lineHuman colon adenocarcinoma cell lineApoptosis signalingEnrichment analysisAldehyde dehydrogenase 1B1Molecular signaturesAdenocarcinoma cell lineMolecular informationSignalingNovel targetProtein expressionCell linesAn AI-powered patient triage platform for future viral outbreaks using COVID-19 as a disease model
Charkoftaki G, Aalizadeh R, Santos-Neto A, Tan W, Davidson E, Nikolopoulou V, Wang Y, Thompson B, Furnary T, Chen Y, Wunder E, Coppi A, Schulz W, Iwasaki A, Pierce R, Cruz C, Desir G, Kaminski N, Farhadian S, Veselkov K, Datta R, Campbell M, Thomaidis N, Ko A, Thompson D, Vasiliou V. An AI-powered patient triage platform for future viral outbreaks using COVID-19 as a disease model. Human Genomics 2023, 17: 80. PMID: 37641126, PMCID: PMC10463861, DOI: 10.1186/s40246-023-00521-4.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsCOVID-19 patientsDisease severityViral outbreaksFuture viral outbreaksLength of hospitalizationIntensive care unitWorse disease prognosisLife-threatening illnessEffective medical interventionsCOVID-19Clinical decision treeGlucuronic acid metabolitesNew potential biomarkersHospitalization lengthCare unitComorbidity dataSerotonin levelsDisease progressionHealthy controlsPatient outcomesDisease prognosisPatient transferPatientsHealthcare resourcesPotential biomarkersFatal Epileptic Seizures in Mice Having Compromised Glutathione and Ascorbic Acid Biosynthesis
Chen Y, Holland K, Shertzer H, Nebert D, Dalton T. Fatal Epileptic Seizures in Mice Having Compromised Glutathione and Ascorbic Acid Biosynthesis. Antioxidants 2023, 12: 448. PMID: 36830006, PMCID: PMC9952205, DOI: 10.3390/antiox12020448.Peer-Reviewed Original ResearchCitationsAltmetricConceptsDKO miceEpileptic seizuresKnockout miceAA supplementationAdult DKO miceFatal epileptic seizuresSpontaneous epileptic seizuresDietary ascorbic acidTissue GSH levelsDouble knockout miceNormal brain functionFunctional crosstalkNeuronal lossHippocampal pathologyGlutamatergic neurotransmissionGlial proliferationBrain damageNeuronal healthPostnatal dayBrain pathologyRate-limiting enzymeSeizuresBrain functionMiceGSH levels
Academic Achievements & Community Involvement
Activities
activity National Institute of Environmental Health Sciences
2024 - PresentPeer Review Groups and Grant Study SectionsAd-hoc reviewerDetailsSuperfund P42 review, Study section ZES1 LWJ-W (CS), ZES1 VSM-W (SF)activity Yale School of Public Health Stolwijk Fellowship
2023 - PresentCommitteesCommittee Member
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Environmental Health Sciences
60 College St, LEPH 521
New Haven, CT 06520
United States
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Yale School of Public Health (LEPH)
Lab
60 College Street, Fl 5th, Rm 508
New Haven, CT 06510