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Angelino Calderone
Researcher at Université de Montréal
Publications - 89
Citations - 3371
Angelino Calderone is an academic researcher from Université de Montréal. The author has contributed to research in topics: Nestin & Muscle hypertrophy. The author has an hindex of 31, co-authored 84 publications receiving 3189 citations. Previous affiliations of Angelino Calderone include Université du Québec & McGill University.
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Interleukin-1 beta modulates the growth and phenotype of neonatal rat cardiac myocytes.
TL;DR: IL-1 beta caused myocyte hypertrophy associated with induction of fetal genes (ANF and beta-MHC) and downregulation of three important calcium regulatory genes (SERCA2, CRC, and VDCC) and may contribute to the abnormal structural and functional alterations of cardiac myocytes in conditions marked by mononuclear cell infiltration.
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Differential Behaviors of Atrial Versus Ventricular Fibroblasts A Potential Role for Platelet-Derived Growth Factor in Atrial-Ventricular Remodeling Differences
TL;DR: Atrial fibroblasts behave differently than ventricular fibro Blasts over a range of in vitro and in vivo paradigms, with atrial Fibroblast showing enhanced reactivity that may explain greater atrial fibrotic responses.
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Regulation of Vascular Endothelial Growth Factor in Cardiac Myocytes
Andrew P. Levy,Nina S. Levy,Joseph Loscalzo,Angelino Calderone,N Takahashi,Kiang-Teck Yeo,Gideon Koren,Wilson S. Colucci,Mark A. Goldberg +8 more
TL;DR: In the present study, VPF/VEGF mRNA and protein were demonstrated to be markedly stimulated in primary rat cardiac myocytes in vitro in response to reduction of the oxygen tension to 1% or inhibition of the electron transport chain, suggesting that more than one signal transduction pathway is involved in regulating VPF-VEGF expression.
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Pressure- and Volume-Induced Left Ventricular Hypertrophies Are Associated With Distinct Myocyte Phenotypes and Differential Induction of Peptide Growth Factor mRNAs
TL;DR: Stimulus-specific heterogeneity in the signaling events and peptide growth factors coupled to gene expression could play a role in determining the type of hypertrophy that is caused by various forms of hemodynamic overload.
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Hypertrophic stimuli induce transforming growth factor-beta 1 expression in rat ventricular myocytes.
TL;DR: The view that TGF-beta 1, released by myocytes and acting in an autocrine and/or paracrine manner, is involved in myocardial remodeling by hypertrophic stimuli is supported.