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Sandra A. Witt

Researcher at Cincinnati Children's Hospital Medical Center

Publications -  63
Citations -  6862

Sandra A. Witt is an academic researcher from Cincinnati Children's Hospital Medical Center. The author has contributed to research in topics: Muscle hypertrophy & Diastole. The author has an hindex of 35, co-authored 63 publications receiving 6486 citations. Previous affiliations of Sandra A. Witt include University of Cincinnati & Boston Children's Hospital.

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The MEK1-ERK1/2 signaling pathway promotes compensated cardiac hypertrophy in transgenic mice.

TL;DR: The results of the present study indicate that the MEK1–ERK1/2 signaling pathway stimulates a physiologic hypertrophy response associated with augmented cardiac function and partial resistance to apoptotsis.
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Temporally Regulated and Tissue-Specific Gene Manipulations in the Adult and Embryonic Heart Using a Tamoxifen-Inducible Cre Protein

TL;DR: MerCreMer transgenic mice represent a tool for temporally regulated inactivation of any loxP-targeted gene within the developing and adult heart or for specifically directing recombination and expression of a lOxP-inactivated cardiac transgene in the heart.
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TGF-β1 mediates the hypertrophic cardiomyocyte growth induced by angiotensin II

TL;DR: TGF-beta1 is an important mediator of the hypertrophic growth response of the heart to Ang II, and the Ang II effect on hypertrophy was shown not to result from stimulation of the endogenous renin-angiotensis system.
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Left ventricular hypertrophy and abnormal ventricular geometry in children and adolescents with obstructive sleep apnea

TL;DR: It is concluded that OSA in children is associated with increased LV mass, and right and left ventricular dimensions and LV mass index and geometry were measured in 28 children with OSA and 19 children with primary snoring.
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The transcription factors GATA4 and GATA6 regulate cardiomyocyte hypertrophy in vitro and in vivo.

TL;DR: A direct functional role for GATA4 and GATA6 as regulators of cardiomyocyte hypertrophic growth and gene expression is demonstrated and it is demonstrated that cardiac-expressed GATA factors are necessary mediators of this process.