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Guillermo Díaz-Araya

Researcher at University of Chile

Publications -  91
Citations -  13233

Guillermo Díaz-Araya is an academic researcher from University of Chile. The author has contributed to research in topics: Receptor & Heart failure. The author has an hindex of 31, co-authored 84 publications receiving 10695 citations. Previous affiliations of Guillermo Díaz-Araya include Pontifical Catholic University of Chile & Valparaiso University.

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FoxO1 mediates TGF-beta1-dependent cardiac myofibroblast differentiation.

TL;DR: It is reported that TGF-β1 stimulates FoxO1 expression, promoting its dephosphorylation, nuclear localization and transcriptional activity in cultured cardiac fibroblasts, and it is proposed thatFoxO1 is an attractive new target for anti-fibrotic therapy.
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A rapid and strong apoptotic process is triggered by hyperosmotic stress in cultured rat cardiac myocytes.

TL;DR: It is suggested that hyperosmotic stress triggers cardiac myocyte apoptosis in a p53-independent manner, being earlier and stronger than apoptosis induced by Doxo and Ang II.
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Antioxidant Effects of 1,4-Dihydropyridine and Nitroso Aryl Derivatives on the Fe+3/Ascorbate-Stimulated Lipid Peroxidation in Rat Brain Slices

TL;DR: All the tested nitroso aryl derivatives were more potent inhibitors of lipid peroxidation than were the parent nitro compounds, and the rank order of antioxidant potency for these derivatives can be established as: ortho-nitrosotoluene>NTP>nitrosobenzene.
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The transcription factor MEF2C mediates cardiomyocyte hypertrophy induced by IGF-1 signaling

TL;DR: It is found that IGF-1 addition to cultured rat cardiomyocytes activated MEF2C, as evidenced by its increased nuclear localization and DNA binding activity, and these novel data suggest that MEf2C activation by IGF- 1 mediates the pro-hypertrophic effects of IGF-2 on cardiac gene expression.
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TGF-β1 prevents simulated ischemia/reperfusion-induced cardiac fibroblast apoptosis by activation of both canonical and non-canonical signaling pathways.

TL;DR: The data suggest that TGF-β1 prevents cardiac fibroblast apoptosis induced by simulated ischemia-reperfusion through the canonical (Smad3) and non canonical (ERK1/2 and Akt) signaling pathways.