2018
Cardiac Hypertrophy: Signaling and Cellular Crosstalk
Tirziu D. Cardiac Hypertrophy: Signaling and Cellular Crosstalk. 2018 DOI: 10.1016/b978-0-12-801238-3.99834-9.Peer-Reviewed Original ResearchCardiac hypertrophyHypertrophic responseHemodynamic stressMolecular basisPathological hypertrophic responsesCellular crosstalkVariety of stimuliMyocardial infarctionImmune cellsCardiac performanceHypertrophic growthChronic increaseVascular cellsPhysiological stimuliCellular communicationMajor playersCardiac cellsWall stressHypertrophyCellsCrosstalkCardiomyocytesPrimary mechanismSignalingStressCardiac Hypertrophy: Signaling and Cellular Crosstalk
Tirziu D. Cardiac Hypertrophy: Signaling and Cellular Crosstalk. 2018, 434-450. DOI: 10.1016/b978-0-12-809657-4.99834-x.Peer-Reviewed Original ResearchCardiac hypertrophyHypertrophic responseHemodynamic stressMolecular basisPathological hypertrophic responsesCellular crosstalkVariety of stimuliMyocardial infarctionImmune cellsCardiac performanceHypertrophic growthChronic increaseVascular cellsPhysiological stimuliCellular communicationMajor playersCardiac cellsWall stressHypertrophyCellsCrosstalkCardiomyocytesPrimary mechanismSignalingStress
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