Yajaira Suarez, PhD
Anthony N. Brady Professor of Comparative Medicine and of Pathology; Deputy Chair, Comparative MedicineCards
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Anthony N. Brady Professor of Comparative Medicine and of Pathology; Deputy Chair, Comparative Medicine
Biography
Yajaira studied Biochemistry and Molecular Biology at the University Autonoma of Madrid (1995). She did her PhD with Miguel Angel Lasuncion at the Hospital Ramón y Cajal and the University Autonoma de Madrid (Spain) (1996-2001). Yajaira also did two post-docs. The first one with Alberto Muñoz at the Instituto de Investigaciones Biomédicas "Alberto Sols" and the Consejo Superior de Investigaciones Científicas-Universidad Autonoma de Madrid (Spain) (2002-2005) and the second one with Jordan Pober and Bill Sessa at Yale University School of Medicine (2005-2009). Yajaira initiated her independent research career in the Division of Cardiology at New York University School of Medicine in 2009. She joined the Yale faculty in 2013 as an Assistant Professor of Comparative Medicine and Pathology. Yajaira is currently Anthony N. Brady Professor of Comparative Medicine and also serves as Deputy Chair for the Department of Comparative Medicine.
Appointments
Comparative Medicine
ProfessorPrimaryPathology
ProfessorSecondary
Other Departments & Organizations
- Cancer Signaling Networks
- Center for RNA Science and Medicine
- Comparative Medicine
- Diabetes Research Center
- Immunology
- Molecular Medicine, Pharmacology, and Physiology
- Obesity Research Working Group
- Pathology
- Pathology and Molecular Medicine
- Pathology Research
- Vascular Biology and Therapeutics Program
- Yale Cancer Center
- Yale Center for Molecular and Systems Metabolism (YMSM)
- Yale Combined Program in the Biological and Biomedical Sciences (BBS)
- Yale Ventures
Education & Training
- PhD
- Universidad Autonoma (2001)
- BS
- Universidad Autonoma (1995)
- Post. Doc.
- Consejo Superior de Investigaciones Científicas (CSIC)-Universidad Autónoma de Madrid
- Post. Doc.
- Yale University School of Medicine
Research
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Overview
In our laboratory we study novel regulatory mechanisms involved in the regulation of endothelial cell and macrophage functions. Both cell types play major role in controlling both angiogenic and inflammatory responses and the interplay between these two cell types has been shown to be critical for several pathophysiological conditions like atherosclerosis, cancer (tumor growth), adipose tissue expansion and wound healing, among others.
To this end, we are utilizing different approaches combining molecular and cellular biology, biochemistry, together with genetically modified mouse models.
Our research program focuses in four different areas:
1) studying the role of non-coding RNAs, including microRNAs, on endothelial cell and macrophage responses to cytokines and growth factors in order to determine the molecular mechanisms that regulates their expression and their overall contribution in regulating angiogenic and inflammatory responses.
2) understanding the implication of endothelial metabolic rewiring on endothelial cell functions
3) understanding the relationship between macrophage inflammatory responses and metabolic regulation (immunometabolism)
4) identifying and characterizing novel mechanisms regulation of cholesterol and lipoprotein metabolism and their involvement in cardiometabolic diseases.
Medical Research Interests
ORCID
0000-0003-4549-2953
Research at a Glance
Yale Co-Authors
Publications Timeline
Research Interests
Carlos Fernandez-Hernando, PhD
Hanming Zhang, PhD
Pablo Fernandez Tussy
Enric Esplugues, PhD
Tamas Horvath, DVM, PhD
Daniel Greif, MD
Atherosclerosis
Cardiovascular Diseases
Inflammation
Publications
Featured Publications
Dynamic metabolism of endothelial triglycerides protects against atherosclerosis in mice
Boutagy N, Gamez-Mendez A, Fowler J, Zhang H, Chaube B, Esplugues E, Kuo A, Lee S, Horikami D, Zhang J, Citrin K, Singh A, Coon B, Lee M, Suarez Y, Fernandez-Hernando C, Sessa W. Dynamic metabolism of endothelial triglycerides protects against atherosclerosis in mice. Journal Of Clinical Investigation 2024, 134: e170453. PMID: 38175710, PMCID: PMC10866653, DOI: 10.1172/jci170453.Peer-Reviewed Original ResearchCitationsAltmetricSuppression of angiopoietin-like 4 reprograms endothelial cell metabolism and inhibits angiogenesis
Chaube B, Citrin K, Sahraei M, Singh A, de Urturi D, Ding W, Pierce R, Raaisa R, Cardone R, Kibbey R, Fernández-Hernando C, Suárez Y. Suppression of angiopoietin-like 4 reprograms endothelial cell metabolism and inhibits angiogenesis. Nature Communications 2023, 14: 8251. PMID: 38086791, PMCID: PMC10716292, DOI: 10.1038/s41467-023-43900-0.Peer-Reviewed Original ResearchCitationsAltmetric
2025
Inflamed endothelial cells express S1PR1 inhibitor CD69 to induce vascular leak
Levesque M, Cartier A, Lin Y, Sah R, Zhang H, Chaube B, Bhaumik M, Körbelin J, Suárez Y, Fernández-Hernando C, Hla T. Inflamed endothelial cells express S1PR1 inhibitor CD69 to induce vascular leak. Journal Of Biological Chemistry 2025, 301: 110455. PMID: 40617350, PMCID: PMC12336701, DOI: 10.1016/j.jbc.2025.110455.Peer-Reviewed Original ResearchAltmetricMeSH Keywords and ConceptsMeSH KeywordsAnimalsAntigens, CDAntigens, Differentiation, T-LymphocyteCapillary PermeabilityEndothelial CellsHumansInflammationInfluenza A Virus, H1N1 SubtypeLectins, C-TypeLungMiceMice, Inbred C57BLOrthomyxoviridae InfectionsReceptors, LysosphingolipidSignal TransductionSphingosine-1-Phosphate ReceptorsConceptsAdeno-associated virus-mediated overexpressionCell surface expressionVascular leakEndothelial cellsIntranasal infectionBarrier functionMouse-adapted influenza virusTight junction protein claudin-5Viral host defenseLung vascular leakSphingosine 1-phosphate receptor 1Protein claudin-5Endothelial cell activationActivation molecule CD69Lung endothelial cellsGenetic mouse modelsEndothelial barrier functionExpression of S1PR1H1N1 infectionInfluenza virusCD69 inductionTLR3 agonistVascular leakageEndothelial activationExaggerated inflammationHypercholesterolemia-induced LXR signaling in smooth muscle cells contributes to vascular lesion remodeling and visceral function
Zhang H, de Urturi D, Fernández-Tussy P, Huang Y, Jovin D, Zhang X, Huang S, Lek M, da Silva Catarino J, Sternak M, Citrin K, Swirski F, Gustafsson J, Greif D, Esplugues E, Biwer L, Suárez Y, Fernández-Hernando C. Hypercholesterolemia-induced LXR signaling in smooth muscle cells contributes to vascular lesion remodeling and visceral function. Proceedings Of The National Academy Of Sciences Of The United States Of America 2025, 122: e2417512122. PMID: 40035761, PMCID: PMC11912459, DOI: 10.1073/pnas.2417512122.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsVascular smooth muscle cellsSmooth muscle cellsLiver X receptorLesion remodelingMuscle cellsVascular functionArterial media layerContribution of lipid metabolismPhenotypic switchingRegulate vascular toneMonocyte-derived macrophagesLipid metabolismPhenotypic switching of vascular smooth muscle cellsSwitching of vascular smooth muscle cellsNecrotic core areaRegulate vascular functionFoam cell populationVisceral myopathyBladder remodelingAortic atheromaFibrous cap thicknessRemodeling in vivoLipid malabsorptionVascular toneAbundant cell type
2024
Intracellular endothelial cell metabolism in vascular function and dysfunction
Citrin K, Chaube B, Fernández-Hernando C, Suárez Y. Intracellular endothelial cell metabolism in vascular function and dysfunction. Trends In Endocrinology And Metabolism 2024, 36: 744-755. PMID: 39672762, PMCID: PMC12159263, DOI: 10.1016/j.tem.2024.11.004.Peer-Reviewed Original ResearchCitationsAltmetricConceptsFatty acid oxidationEndothelial cellsIntracellular metabolic pathwaysInner lining of blood vesselsVascular functionCell metabolismMetabolic pathwaysEndothelial cell metabolismLipid handlingDesign new therapiesRegulate vascular toneInfluence disease progressionAcid oxidationMetabolic signaturesVascular toneNew therapiesLining of blood vesselsDisease progressionLeukocyte adhesionMetabolic changesVascular diseaseOxidative stressBlood vesselsIncreased permeabilityWound healingmiR-33 deletion in hepatocytes attenuates NAFLD-NASH-HCC progression
Fernández-Tussy P, Cardelo M, Zhang H, Sun J, Price N, Boutagy N, Goedeke L, Cadena-Sandoval M, Xirouchaki C, Brown W, Yang X, Pastor-Rojo O, Haeusler R, Bennett A, Tiganis T, Suárez Y, Fernández-Hernando C. miR-33 deletion in hepatocytes attenuates NAFLD-NASH-HCC progression. JCI Insight 2024, 9: e168476. PMID: 39190492, PMCID: PMC11466198, DOI: 10.1172/jci.insight.168476.Peer-Reviewed Original ResearchCitationsAltmetricConceptsMiR-33Regulation of biological processesMitochondrial fatty acid oxidationRegulation of lipid metabolismNon-alcoholic fatty liver diseaseDevelopment of effective therapeuticsFatty acid oxidationLipid synthesisProgression of non-alcoholic fatty liver diseaseMitochondrial functionTarget genesBiological processesComplex diseasesNon-alcoholic steatohepatitisLipid accumulationDeletionDevelopment of non-alcoholic fatty liver diseasePathway activationLipid metabolismProgress to non-alcoholic steatohepatitisAcid oxidationHCC progressionEffective therapeuticsTherapeutic targetHepatocellular carcinomaAbstract 129: Hypercholesterolemia-induced Lxr Signaling In Smc Contributes To Atherosclerotic Lesion Remodeling And Regulates Vascular And Visceral Smc Function
Zhang H, Biwer L, de Urturi D, Fernandez-Tussy P, Jovin D, Huang Y, Zhang X, Esplugues E, Greif D, Suarez Y, Fernandez-Hernando C. Abstract 129: Hypercholesterolemia-induced Lxr Signaling In Smc Contributes To Atherosclerotic Lesion Remodeling And Regulates Vascular And Visceral Smc Function. Arteriosclerosis Thrombosis And Vascular Biology 2024, 44: a129-a129. DOI: 10.1161/atvb.44.suppl_1.129.Peer-Reviewed Original ResearchCitationsConceptsLiver X receptorTranscription factorsVascular smooth muscle cellsRegulation of lipid metabolismLXR signalingB geneScRNA-seqFate decisionsSignaling eventsSMC functionGene expressionActivation of liver X receptorCell statesLesion remodelingCharacterized miceLipid metabolismLineage tracingPhenotypic switchingX receptorReduced fibrous cap thicknessTranscriptionFeatures of plaque instabilitySmooth muscle cellsLipid absorptionProgression of atherosclerosisFatty acid binding protein 5 suppression attenuates obesity-induced hepatocellular carcinoma by promoting ferroptosis and intratumoral immune rewiring
Sun J, Esplugues E, Bort A, Cardelo M, Ruz-Maldonado I, Fernández-Tussy P, Wong C, Wang H, Ojima I, Kaczocha M, Perry R, Suárez Y, Fernández-Hernando C. Fatty acid binding protein 5 suppression attenuates obesity-induced hepatocellular carcinoma by promoting ferroptosis and intratumoral immune rewiring. Nature Metabolism 2024, 6: 741-763. PMID: 38664583, PMCID: PMC12355809, DOI: 10.1038/s42255-024-01019-6.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsFatty acid binding protein 5Tumor-associated macrophagesHepatocellular carcinomaImmunosuppressive phenotype of tumor-associated macrophagesIncreased CD8+ T cell activationCD8+ T cell activationPhenotype of tumor-associated macrophagesPro-inflammatory tumor microenvironmentCo-stimulatory molecules CD80T cell activationHepatocellular carcinoma burdenTransformation of hepatocytesBinding protein 5Potential therapeutic approachImmunosuppressive phenotypeTumor microenvironmentFerroptosis-induced cell deathMale miceEnhanced ferroptosisTherapeutic approachesPharmacological inhibitionGenetic ablationIncreased expressionSingle-cell atlasAnalysis of transformed cellsmicroRNA-33 controls hunger signaling in hypothalamic AgRP neurons
Price N, Fernández-Tussy P, Varela L, Cardelo M, Shanabrough M, Aryal B, de Cabo R, Suárez Y, Horvath T, Fernández-Hernando C. microRNA-33 controls hunger signaling in hypothalamic AgRP neurons. Nature Communications 2024, 15: 2131. PMID: 38459068, PMCID: PMC10923783, DOI: 10.1038/s41467-024-46427-0.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsAgRP neuronsFeeding behaviorFatty acid metabolismNon-coding RNAsMitochondrial biogenesisRegulatory pathwaysTarget genesHypothalamic AgRP neuronsExcessive nutrient intakeCentral regulatorBioenergetic processesAcid metabolismActivation of AgRP neuronsModulate feeding behaviorCentral regulation of feeding behaviorRegulation of feeding behaviorMiR-33Hunger signalsMicroRNA-33Metabolic diseasesAlternative therapeutic approachLoss of miR-33Mouse modelMetabolic dysfunctionRegulationHeterogeneity of hepatocyte dynamics restores liver architecture after chemical, physical or viral damage
Ruz-Maldonado I, Gonzalez J, Zhang H, Sun J, Bort A, Kabir I, Kibbey R, Suárez Y, Greif D, Fernández-Hernando C. Heterogeneity of hepatocyte dynamics restores liver architecture after chemical, physical or viral damage. Nature Communications 2024, 15: 1247. PMID: 38341404, PMCID: PMC10858916, DOI: 10.1038/s41467-024-45439-0.Peer-Reviewed Original ResearchCitationsAltmetric
Academic Achievements & Community Involvement
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Honors
honor 2025 Recipient of the Judah Folkman Award in Vascular Biology
02/13/2025International AwardNorth American Vascular Biology Organization (NAVBO)honor Elected member of Connecticut Academy of Science and Engineering
02/21/2022Regional AwardConnecticut Academy of Science and Engineeringhonor Werner Risau New Investigator Award in Vascular Biology
International AwardAmerican Heart Association- Journal Arteriosclerosis, Thrombosis and Vascular Biology.DetailsUnited Stateshonor Kingsley Award in Medical Research
Yale School of Medicine AwardDetailsUnited Stateshonor Fellowship-Grant Award, CNIC P3+3 programme for Post-doctoral Careers in Biomedicine.
International AwardFundación Centro Nacional de Investigaciones Cardiovasculares Carlos III, SpainDetailsUnited States
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Yale Only Arif Yurdagul, PhD