Featured Publications
Complement C1q-induced activation of β-catenin signalling causes hypertensive arterial remodelling
Sumida T, Naito AT, Nomura S, Nakagawa A, Higo T, Hashimoto A, Okada K, Sakai T, Ito M, Yamaguchi T, Oka T, Akazawa H, Lee JK, Minamino T, Offermanns S, Noda T, Botto M, Kobayashi Y, Morita H, Manabe I, Nagai T, Shiojima I, Komuro I. Complement C1q-induced activation of β-catenin signalling causes hypertensive arterial remodelling. Nature Communications 2015, 6: 6241. PMID: 25716000, PMCID: PMC4351572, DOI: 10.1038/ncomms7241.Peer-Reviewed Original ResearchConceptsVascular smooth muscle cellsProliferation of VSMCsArterial remodellingΒ-catenin signalingΒ-cateninComplement C1qBlood pressure elevationEnd-organ damageNovel therapeutic targetSmooth muscle cellsMacrophage depletionImmune cellsPrecise molecular mechanismsTherapeutic targetStructural remodellingMuscle cellsRemodellingHypertensionArteriosclerosisComplement C1ActivationC1qMolecular mechanismsSignalingGene deletionHyperosmotic stress response regulates interstitial homeostasis and pathogenic inflammation
Sumida T. Hyperosmotic stress response regulates interstitial homeostasis and pathogenic inflammation. The Journal Of Biochemistry 2023, 173: 159-166. PMID: 36722164, DOI: 10.1093/jb/mvad009.Peer-Reviewed Original ResearchConceptsHyperosmotic stress responseStress responseCell type-specific mannerFundamental cellular responsesType-specific mannerHeat shock proteinsCell cycle arrestImmune cell differentiationOsmolyte synthesisContext of diseaseHyperosmotic stressIon transportersHyperosmotic responseMetabolic remodelingMolecular mechanismsCellular responsesShock proteinsCell differentiationHuman diseasesCellular shrinkageCycle arrestAdaptative responseSpecific mannerTissue microenvironmentTissue immune homeostasis
2024
An autoimmune transcriptional circuit drives FOXP3+ regulatory T cell dysfunction
Sumida T, Lincoln M, He L, Park Y, Ota M, Oguchi A, Son R, Yi A, Stillwell H, Leissa G, Fujio K, Murakawa Y, Kulminski A, Epstein C, Bernstein B, Kellis M, Hafler D. An autoimmune transcriptional circuit drives FOXP3+ regulatory T cell dysfunction. Science Translational Medicine 2024, 16: eadp1720. PMID: 39196959, DOI: 10.1126/scitranslmed.adp1720.Peer-Reviewed Original ResearchConceptsForkhead box P3Autoimmune diseasesCD4<sup>+</sup>Foxp3<sup>+</sup> regulatory T cellsMultiple sclerosisFoxp3<sup>+</sup> regulatory T cellsRegulatory T cell dysfunctionPR domain zinc finger protein 1Zinc finger protein 1Glucocorticoid-regulated kinase 1Regulatory T cellsT cell dysfunctionDisorder of young adultsAutoimmune disease multiple sclerosisDisease multiple sclerosisExpression of serumTranscriptional circuitsEpigenomic profilingShort isoformPrevent autoimmunityUpstream regulatorT cellsHuman autoimmunityEvolutionary emergenceKinase 1Molecular mechanisms
2019
Activation of DNA Damage Response and Cellular Senescence in Cardiac Fibroblasts Limit Cardiac Fibrosis After Myocardial Infarction
Shibamoto M, Higo T, Naito AT, Nakagawa A, Sumida T, Okada K, Sakai T, Kuramoto Y, Yamaguchi T, Ito M, Masumura Y, Higo S, Lee JK, Hikoso S, Komuro I, Sakata Y. Activation of DNA Damage Response and Cellular Senescence in Cardiac Fibroblasts Limit Cardiac Fibrosis After Myocardial Infarction. International Heart Journal 2019, 60: 944-957. PMID: 31257341, DOI: 10.1536/ihj.18-701.Peer-Reviewed Original ResearchConceptsCellular senescenceDNA damage response systemDNA damage responseCardiac fibroblastsDDR activationDamage responseMolecular mechanismsSenescenceGene deletionJuxtacrine mannerProliferation of CFsCardiac fibrosisCF proliferationProliferationCardiac remodelingActivationTissue fibrosisRemodelingImportant roleTherapeutic strategiesRoleRecent reportsDeletionRegulationATM gene deletion
2010
Promotion of CHIP-Mediated p53 Degradation Protects the Heart From Ischemic Injury
Naito AT, Okada S, Minamino T, Iwanaga K, Liu ML, Sumida T, Nomura S, Sahara N, Mizoroki T, Takashima A, Akazawa H, Nagai T, Shiojima I, Komuro I. Promotion of CHIP-Mediated p53 Degradation Protects the Heart From Ischemic Injury. Circulation Research 2010, 106: 1692-1702. PMID: 20413784, DOI: 10.1161/circresaha.109.214346.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAnimals, NewbornApoptosisBase SequenceBenzoquinonesCell HypoxiaChlorocebus aethiopsCOS CellsDisease Models, AnimalGenetic TherapyHSP90 Heat-Shock ProteinsHumansHypoxia-Inducible Factor 1, alpha SubunitLactams, MacrocyclicMaleMiceMice, Inbred C57BLMice, KnockoutMolecular Sequence DataMutationMyocardial InfarctionMyocytes, CardiacPromoter Regions, GeneticProteasome Endopeptidase ComplexProtein Processing, Post-TranslationalRatsRats, WistarRNA InterferenceTranscriptional ActivationTumor Suppressor Protein p53UbiquitinationUbiquitin-Protein LigasesVentricular RemodelingConceptsMyocardial infarctionP53 accumulationCardiomyocyte apoptosisCoronary heart diseaseNumber of patientsNovel therapeutic strategiesP53 degradationApoptosis of cardiomyocytesHeat shock proteinsHeart failureIschemic injuryCardioprotective effectsVentricular remodelingCHIP overexpressionHeart diseaseInfarctionTherapeutic strategiesProteasomal degradationMyocardial apoptosisAmount of p53Molecular mechanismsShock proteinsP53 antagonistP53 accumulatesProtein levels