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 deletion
2015
Angiotensin II receptor blockade promotes repair of skeletal muscle through down-regulation of aging-promoting C1q expression
Yabumoto C, Akazawa H, Yamamoto R, Yano M, Kudo-Sakamoto Y, Sumida T, Kamo T, Yagi H, Shimizu Y, Saga-Kamo A, Naito AT, Oka T, Lee JK, Suzuki J, Sakata Y, Uejima E, Komuro I. Angiotensin II receptor blockade promotes repair of skeletal muscle through down-regulation of aging-promoting C1q expression. Scientific Reports 2015, 5: 14453. PMID: 26571361, PMCID: PMC4585890, DOI: 10.1038/srep14453.Peer-Reviewed Original ResearchMeSH KeywordsAdministration, TopicalAgingAngiotensin II Type 1 Receptor BlockersAnimalsAxin ProteinBiphenyl CompoundsCell LineComplement C1qDown-RegulationImmunohistochemistryIrbesartanMacrophagesMaleMiceMice, Inbred C57BLMice, KnockoutMuscle, SkeletalPAX7 Transcription FactorReceptor, Angiotensin, Type 1RegenerationTetrazolesWnt Signaling PathwayConceptsC1q expressionReceptor blockadeAge-related declineAngiotensin II receptor blockadeAT1 receptor blocker irbesartanAngiotensin II type 1 receptorII type 1 receptorAT1 receptor blockadeFunctional muscle recoveryII receptor blockadeSkeletal muscleReceptor blocker irbesartanType 1 receptorWnt/β-catenin pathwaySkeletal muscle functionWnt/β-catenin signalingMuscle regenerationΒ-catenin pathwayCultured macrophage cellsΒ-catenin signalingAT1 receptorMuscle recoveryM2 polarizationMuscle functionTopical administration
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