Genta Ishikawa, MD, MPH
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Research
Publications
2025
Cyclic GMP-AMP synthase expression is enhanced in systemic sclerosis-associated interstitial lung disease and stimulates inflammatory myofibroblast activation
Yu S, Hu B, Sun Y, Peng X, Lee C, Woo S, McGovern J, Zielonka J, Saber T, Ghincea A, Gandhi S, Walia A, Pivarnik T, Ishikawa G, Shao S, Sun H, Gunes B, Kujawski S, Perez S, Odell W, Hinchcliff M, Varga J, Feghali-Bostwick C, Sauler M, Gomez J, Ryu C, Herzog E. Cyclic GMP-AMP synthase expression is enhanced in systemic sclerosis-associated interstitial lung disease and stimulates inflammatory myofibroblast activation. European Respiratory Journal 2025, 66: 2401564. PMID: 40374521, PMCID: PMC12332468, DOI: 10.1183/13993003.01564-2024.Peer-Reviewed Original ResearchPrecision cut lung slicesSSc-ILD lung tissuesType 1 interferonSSc-ILDProduction of cytokinesBronchoalveolar lavageHuman precision cut lung slicesLung tissueLung fibroblastsLungs of patientsInterstitial lung diseasePulmonary fibrosis modelBleomycin mouse modelIsolated lung fibroblastsCultured fibroblastsPerturbs innate immunityFibrotic stimuliSingle cell RNA sequencing datasetsSystemic sclerosisHuman lung fibroblastsLung diseaseMouse modelCyclic GMP-AMP synthaseFibrosis modelTherapeutic approachesDamage sensing through TLR9 regulates inflammatory and antiviral responses during influenza infection
Kim J, Yuan Y, Agaronyan K, Zhao A, Wang V, Gau D, Toosi N, Gupta G, Essayas H, Kaminski A, McGovern J, Yu S, Woo S, Lee C, Gandhi S, Saber T, Saleh T, Hu B, Sun Y, Ishikawa G, Bain W, Evankovich J, Chen L, Yun H, Herzog E, Dela Cruz C, Ryu C, Sharma L. Damage sensing through TLR9 regulates inflammatory and antiviral responses during influenza infection. Mucosal Immunology 2025, 18: 537-548. PMID: 39884393, PMCID: PMC12205908, DOI: 10.1016/j.mucimm.2025.01.008.Peer-Reviewed Original ResearchToll-like receptor 9Anti-influenza immunityToll-like receptor 9 activationImpaired viral clearanceViral clearanceMyeloid cellsTissue injuryInflammatory responseInfluenza infectionPersistent inflammationLung injuryTissue damageToll-like receptor 9 deficiencyReceptor 9Toll-like receptor 9 signalingToll-like receptor 9 ligandInfection of immune cellsInfluenza-infected individualsPersistent lung injuryTLR9-/- miceInfected myeloid cellsInflammatory lung injurySensing tissue damageUnmethylated CpG DNA sequencesMitochondrial DNAToll-like Receptor 9 Inhibition Mitigates Fibroproliferative Responses in Translational Models of Pulmonary Fibrosis
Trujillo G, Regueiro-Ren A, Liu C, Hu B, Sun Y, Ahangari F, Fiorini V, Ishikawa G, Al Jumaily K, Khoury J, McGovern J, Lee C, Peng X, Pivarnik T, Sun H, Walia A, Woo S, Yu S, Antin-Ozerkis D, Sauler M, Kaminski N, Herzog E, Ryu C. Toll-like Receptor 9 Inhibition Mitigates Fibroproliferative Responses in Translational Models of Pulmonary Fibrosis. American Journal Of Respiratory And Critical Care Medicine 2025, 211: 91-102. PMID: 39189851, PMCID: PMC11755360, DOI: 10.1164/rccm.202401-0065oc.Peer-Reviewed Original ResearchToll-like receptor 9Model of pulmonary fibrosisIdiopathic pulmonary fibrosisPulmonary fibrosisFibroproliferative responseLung diseaseIdiopathic pulmonary fibrosis cohortsExpression of toll-like receptor 9Toll-like receptor 9 activationTransplant-free survivalExpression of MCP-1Cohort of patientsSlow clinical progressionFibrotic lung diseaseAccelerated disease courseFatal lung diseaseIP-10Pharmacodynamic endpointsPreclinical modelsDisease courseClinical progressionPlasma mtDNAMCP-1Receptor 9Mouse model
2024
Single-Cell Profiling Reveals Immune Aberrations in Progressive Idiopathic Pulmonary Fibrosis.
Unterman A, Zhao A, Neumark N, Schupp J, Ahangari F, Cosme C, Sharma P, Flint J, Stein Y, Ryu C, Ishikawa G, Sumida T, Gomez J, Herazo-Maya J, Dela Cruz C, Herzog E, Kaminski N. Single-Cell Profiling Reveals Immune Aberrations in Progressive Idiopathic Pulmonary Fibrosis. American Journal Of Respiratory And Critical Care Medicine 2024, 210: 484-496. PMID: 38717443, PMCID: PMC11351796, DOI: 10.1164/rccm.202306-0979oc.Peer-Reviewed Original ResearchStable idiopathic pulmonary fibrosisIdiopathic pulmonary fibrosisPeripheral blood mononuclear cellsProgressive idiopathic pulmonary fibrosisPeripheral immune systemT cellsPulmonary fibrosisCohort of IPF patientsAssociated with decreased survivalIdiopathic pulmonary fibrosis patientsPeripheral blood mononuclear cell samplesPeripheral blood cell populationsImmune systemFraction of TregsRegulatory T cellsBlood mononuclear cellsBlood cell populationsFlow cytometry analysisImmune aberrationsIPF patientsTregsMononuclear cellsSingle-cell RNA sequencingLung homogenatesMonocyte chemoattractant
2023
α1 Adrenoreceptor antagonism mitigates extracellular mitochondrial DNA accumulation in lung fibrosis models and in patients with idiopathic pulmonary fibrosis
Ishikawa G, Peng X, McGovern J, Woo S, Perry C, Liu A, Yu S, Ghincea A, Kishchanka A, Fiorini V, Hu B, Sun Y, Sun H, Ryu C, Herzog E. α1 Adrenoreceptor antagonism mitigates extracellular mitochondrial DNA accumulation in lung fibrosis models and in patients with idiopathic pulmonary fibrosis. American Journal Of Physiology - Lung Cellular And Molecular Physiology 2023, 324: l639-l651. PMID: 36648147, PMCID: PMC10110730, DOI: 10.1152/ajplung.00119.2022.Peer-Reviewed Original ResearchConceptsAdrenergic nerve supplyIdiopathic pulmonary fibrosisΑ1 adrenoreceptorsPulmonary fibrosisNerve supplyCultured normal human lung fibroblastsInnate immune ligandsLung fibrosis modelNormal human lung fibroblastsSmooth muscle actinHuman lung fibroblastsAdrenal resectionAdrenoreceptor antagonismExtracellular mtDNAIPF cohortImproved survivalΑ1-adrenoreceptor antagonistsLung fibrosisAdrenal sourceFibroblast accumulationAdrenoreceptor antagonistBleomycin modelFibrosis modelLung fibrogenesisMouse model
2022
PTX3 in Granuloma Formation and Sarcoidosis: Helping Macrophages Accept a “Complement”
Ishikawa G, Herzog EL. PTX3 in Granuloma Formation and Sarcoidosis: Helping Macrophages Accept a “Complement”. American Journal Of Respiratory And Critical Care Medicine 2022, 206: 1064-1065. PMID: 35820078, PMCID: PMC9704837, DOI: 10.1164/rccm.202207-1277ed.Commentaries, Editorials and Letters
2021
Evolving Perspectives on Innate Immune Mechanisms of IPF
Ishikawa G, Liu A, Herzog EL. Evolving Perspectives on Innate Immune Mechanisms of IPF. Frontiers In Molecular Biosciences 2021, 8: 676569. PMID: 34434962, PMCID: PMC8381017, DOI: 10.3389/fmolb.2021.676569.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsIdiopathic pulmonary fibrosisInnate immunityInnate immune populationsMolecular patternsMyeloid suppressor cellsInnate lymphoid cellsInnate immune mechanismsEpithelial-fibroblast interactionsRole of substancesSuppressor cellsPulmonary fibrosisImmune populationsImmune mechanismsDisease outcomePotential therapyLymphoid cellsHuman studiesFibrotic microenvironmentCommensal microbesAnimal modelingGenetic factorsImmunityFuture studiesComplex roleCellsElevated IL-15 concentrations in the sarcoidosis lung are independent of granuloma burden and disease phenotypes
Minasyan M, Sharma L, Pivarnik T, Liu W, Adams T, Bermejo S, Peng X, Liu A, Ishikawa G, Perry C, Kaminski N, Gulati M, Herzog EL, Dela Cruz CS, Ryu C. Elevated IL-15 concentrations in the sarcoidosis lung are independent of granuloma burden and disease phenotypes. American Journal Of Physiology - Lung Cellular And Molecular Physiology 2021, 320: l1137-l1146. PMID: 33851886, PMCID: PMC8285626, DOI: 10.1152/ajplung.00575.2020.Peer-Reviewed Original ResearchConceptsIL-15 concentrationsIL-15Bronchoalveolar lavageDisease pathogenesisSarcoidosis lungClinical manifestationsLineages of miceIL-15 receptor αHuman cohortsInflammation of sarcoidosisIL-15 levelsOngoing inflammatory processSystemic granulomatous diseaseNumber of granulomasDisease phenotypeSarcoidosis cohortTDM administrationGranuloma numberComorbid conditionsClinical progressionInterleukin-15Granulomatous diseaseInflammatory processGranuloma formationHealthy controlsMacrophage-derived netrin-1 drives adrenergic nerve–associated lung fibrosis
Gao R, Peng X, Perry C, Sun H, Ntokou A, Ryu C, Gomez JL, Reeves BC, Walia A, Kaminski N, Neumark N, Ishikawa G, Black KE, Hariri LP, Moore MW, Gulati M, Homer RJ, Greif DM, Eltzschig HK, Herzog EL. Macrophage-derived netrin-1 drives adrenergic nerve–associated lung fibrosis. Journal Of Clinical Investigation 2021, 131: e136542. PMID: 33393489, PMCID: PMC7773383, DOI: 10.1172/jci136542.Peer-Reviewed Original ResearchConceptsNetrin-1Lung fibrosisCell-specific knockout miceΑ1-adrenoreceptor blockadeIPF lung tissueNeuronal guidance proteinsNetrin-1 expressionExtracellular matrix accumulationAdrenergic processesAdrenoreceptor antagonismAdrenoreceptor blockadeFibrotic histologyInflammatory scarringIPF cohortAdrenergic nervesΑ1-blockersImproved survivalColorectal carcinomaLung tissueKnockout miceCollagen accumulationFibrosisMatrix accumulationMacrophagesGuidance proteins
2019
Shared and Tissue-Specific Expression Signatures between Bone Marrow from Primary Myelofibrosis and Essential Thrombocythemia
Ishikawa G, Fujiwara N, Hirschfield H, Varricchio L, Hoshida Y, Barosi G, Rosti V, Padilla M, Mazzarini M, Friedman SL, Hoffman R, Migliaccio AR. Shared and Tissue-Specific Expression Signatures between Bone Marrow from Primary Myelofibrosis and Essential Thrombocythemia. Experimental Hematology 2019, 79: 16-25.e3. PMID: 31678370, PMCID: PMC6910948, DOI: 10.1016/j.exphem.2019.10.001.Peer-Reviewed Original ResearchConceptsBone marrowLung fibrosisMyeloproliferative neoplasmsEssential thrombocytopeniaLiver fibrosisPhiladelphia-negative myeloproliferative neoplasmsProtein 1Possible therapeutic targetPrimary myelofibrosis patientsExpression of Id1Extracellular matrix protein 1Poor prognosisIL-8Myelofibrosis patientsEssential thrombocythemiaTherapeutic targetPrimary myelofibrosisFibrosisMegakaryocyte hyperplasiaCholesterol homeostasisBM functionHematopoietic failureMatrix protein 1K-rasPotential target
Academic Achievements & Community Involvement
Clinical Care
Overview
Genta Ishikawa, MD, is a pulmonologist who cares for people with interstitial lung disease, including pulmonary fibrosis, a form of lung scarring. He also provides critical care support for patients who experience severe respiratory challenges.
As an instructor at Yale School of Medicine, Dr. Ishikawa studies how nerve-derived chemicals such as noradrenaline influence lung scarring, with the goal of discovering new ways to slow or halt disease progression.
Dr. Ishikawa earned his medical degree from Hokkaido University in Japan and completed a master of public health at Emory University. He went on to finish a residency in internal medicine and a fellowship in pulmonary, critical care, and sleep medicine at Mount Sinai in New York, followed by a postdoctoral fellowship at Yale School of Medicine.
Clinical Specialties
Internal Medicine; Pulmonary Critical Care ; Critical Care Medicine
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Pulmonary, Critical Care & Sleep Medicine
300 Cedar Street, P.O. Box 208057
New Haven, CT 06520
United States
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