Featured Publications
Complement C1q Activates Canonical Wnt Signaling and Promotes Aging-Related Phenotypes
Naito AT, Sumida T, Nomura S, Liu ML, Higo T, Nakagawa A, Okada K, Sakai T, Hashimoto A, Hara Y, Shimizu I, Zhu W, Toko H, Katada A, Akazawa H, Oka T, Lee JK, Minamino T, Nagai T, Walsh K, Kikuchi A, Matsumoto M, Botto M, Shiojima I, Komuro I. Complement C1q Activates Canonical Wnt Signaling and Promotes Aging-Related Phenotypes. Cell 2012, 149: 1298-1313. PMID: 22682250, PMCID: PMC3529917, DOI: 10.1016/j.cell.2012.03.047.Peer-Reviewed Original ResearchConceptsComplement C1qWnt coreceptor low-density lipoprotein receptor-related protein 6Canonical Wnt signalingLow-density lipoprotein receptor-related protein 6Serum C1q concentrationLipoprotein receptor-related protein 6Age-related phenotypesWild-type miceAge-associated impairmentWnt signalingMuscle regenerationAge-associated declineYoung miceC1q treatmentC1q concentrationsSkeletal muscle regenerationMammalian agingMiceProtein 6C1qC1s inhibitionCanonical WntMultiple tissuesFrizzled receptorsWntComplement 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
Wnt/&bgr;-Catenin Signaling Contributes to Skeletal Myopathy in Heart Failure via Direct Interaction With Forkhead Box O
Okada K, Naito AT, Higo T, Nakagawa A, Shibamoto M, Sakai T, Hashimoto A, Kuramoto Y, Sumida T, Nomura S, Ito M, Yamaguchi T, Oka T, Akazawa H, Lee JK, Morimoto S, Sakata Y, Shiojima I, Komuro I. Wnt/&bgr;-Catenin Signaling Contributes to Skeletal Myopathy in Heart Failure via Direct Interaction With Forkhead Box O. Circulation Heart Failure 2015, 8: 799-808. PMID: 26038536, DOI: 10.1161/circheartfailure.114.001958.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBeta CateninCardiomyopathy, DilatedCell LineComplement C1qDisease Models, AnimalForkhead Box Protein O1Forkhead Transcription FactorsMice, TransgenicMuscle FatigueMuscle Fibers, SkeletalMuscle, SkeletalMuscular DiseasesRNA InterferenceTransfectionWnt Signaling PathwayWnt3A ProteinConceptsChronic heart failureFiber type shiftFatigable fibersSkeletal myopathyActivation of WntHeart failureModel miceCardiomyopathy miceSkeletal muscleNovel therapeutic targetMediator β-cateninType IIB fibersControl miceType shiftC2C12 cellsTherapeutic targetSignaling contributesComplement C1qMyopathyMiceCritical roleIIB fibersForkhead box OΒ-cateninFoxO1 activity