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
2015
A Food-Derived Flavonoid Luteolin Protects against Angiotensin II-Induced Cardiac Remodeling
Nakayama A, Morita H, Nakao T, Yamaguchi T, Sumida T, Ikeda Y, Kumagai H, Motozawa Y, Takahashi T, Imaizumi A, Hashimoto T, Nagai R, Komuro I. A Food-Derived Flavonoid Luteolin Protects against Angiotensin II-Induced Cardiac Remodeling. PLOS ONE 2015, 10: e0137106. PMID: 26327560, PMCID: PMC4556625, DOI: 10.1371/journal.pone.0137106.Peer-Reviewed Original ResearchMeSH KeywordsAngiotensin IIAnimalsAntioxidantsAtrial Natriuretic FactorConnective Tissue Growth FactorDietFibroblastsFibrosisFlavonoidsFoodHeartHydrogen PeroxideHypertrophyLuteolinMaleMyocardiumOxidative StressPhosphorylationRatsRats, Sprague-DawleySignal TransductionTransforming Growth Factor beta1Ventricular RemodelingConceptsCardiac remodelingAng IIOral pretreatmentII-Induced Cardiac RemodelingOxidative stressCultured rat cardiac fibroblastsRat cardiac fibroblastsPhosphorylation of JNKHyperoxidative stateAntifibrotic effectsCardiac fibrosisCardiac functionLuteolin pretreatmentTGFβ1 expressionCardiac fibroblastsPotent antioxidantHerbal extractsProtective actionCardiac tissueRemodelingExpression levelsGene expression levelsDietPretreatmentProtective properties
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