2016
miR-182 Modulates Myocardial Hypertrophic Response Induced by Angiogenesis in Heart
Li N, Hwangbo C, Jaba IM, Zhang J, Papangeli I, Han J, Mikush N, Larrivée B, Eichmann A, Chun HJ, Young LH, Tirziu D. miR-182 Modulates Myocardial Hypertrophic Response Induced by Angiogenesis in Heart. Scientific Reports 2016, 6: 21228. PMID: 26888314, PMCID: PMC4758045, DOI: 10.1038/srep21228.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCardiomegalyEndotheliumMechanistic Target of Rapamycin Complex 1Membrane ProteinsMiceMice, KnockoutMicroRNAsMultiprotein ComplexesMyocytes, CardiacNeovascularization, PathologicNitric OxideNitric Oxide Synthase Type IIIProteinsProto-Oncogene Proteins c-aktRGS ProteinsTOR Serine-Threonine KinasesUp-RegulationConceptsHypertrophic responseMiR-182Myocardial hypertrophyEndothelial-cardiomyocyte crosstalkLV pressure overloadEndothelium-derived NOPlacental growth factorMyocardial hypertrophic responseDevelopment of hypertrophyDegradation of regulatorsMiR-182 targetsHemodynamic demandsPressure overloadPlGF expressionBlood supplyParacrine actionCardiomyocyte hypertrophyMyocardial angiogenesisCardiac angiogenesisTreatment inhibitsHypertrophyAKT/mTORC1 pathwaysNovel targetAkt/Growth factor
2010
Cell Communications in the Heart
Tirziu D, Giordano FJ, Simons M. Cell Communications in the Heart. Circulation 2010, 122: 928-937. PMID: 20805439, PMCID: PMC2941440, DOI: 10.1161/circulationaha.108.847731.Peer-Reviewed Original Research
2008
Endothelium-Driven Myocardial Growth or Nitric Oxide at the Crossroads
Tirziu D, Simons M. Endothelium-Driven Myocardial Growth or Nitric Oxide at the Crossroads. Trends In Cardiovascular Medicine 2008, 18: 299-305. PMID: 19345317, PMCID: PMC2692333, DOI: 10.1016/j.tcm.2009.01.002.Peer-Reviewed Original ResearchAnimalsBlood Coagulation FactorsCardiomegalyCoronary CirculationEndothelinsEndothelium, VascularFibroblast Growth FactorsHumansIon Channel GatingMyocardiumMyocytes, CardiacNitric OxideNitric Oxide Synthase Type INitric Oxide Synthase Type IIIParacrine CommunicationPlatelet-Derived Growth FactorProstaglandinsSignal TransductionVascular Endothelial Growth Factors
2007
Myocardial hypertrophy in the absence of external stimuli is induced by angiogenesis in mice
Tirziu D, Chorianopoulos E, Moodie KL, Palac RT, Zhuang ZW, Tjwa M, Roncal C, Eriksson U, Fu Q, Elfenbein A, Hall AE, Carmeliet P, Moons L, Simons M. Myocardial hypertrophy in the absence of external stimuli is induced by angiogenesis in mice. Journal Of Clinical Investigation 2007, 117: 3188-3197. PMID: 17975666, PMCID: PMC2045601, DOI: 10.1172/jci32024.Peer-Reviewed Original ResearchMeSH KeywordsAngiogenic ProteinsAnimalsCardiomegalyCells, CulturedEchocardiographyEndothelial CellsEnzyme InhibitorsHeartHemodynamicsMiceMice, Inbred C57BLMice, TransgenicMyocardiumMyocytes, CardiacNeovascularization, PhysiologicNG-Nitroarginine Methyl EsterOrgan SizeRatsRats, Sprague-DawleyTransgenesConceptsMyocardial hypertrophyHeart sizeNormal heart sizeENOS inhibitor L-NAMEInhibitor L-NAMEAtrial natriuretic factorHypertrophic marker expressionNormal adult mouse heartAdult mouse heartAngiogenic growth factorsL-NAMEBeta-MHCCardiac massMyocardial infarctionMyocardial functionNatriuretic factorCardiac performanceCardiomyocyte sizeTransgenic miceStimulation periodHeart growthHypertrophy markersMarker expressionMouse heartsMurine heart