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Sawa Kostin

Researcher at Max Planck Society

Publications -  142
Citations -  14920

Sawa Kostin is an academic researcher from Max Planck Society. The author has contributed to research in topics: Myocyte & Apoptosis. The author has an hindex of 60, co-authored 142 publications receiving 13812 citations. Previous affiliations of Sawa Kostin include University of Göttingen & University of Hawaii at Manoa.

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Progression From Compensated Hypertrophy to Failure in the Pressure-Overloaded Human Heart Structural Deterioration and Compensatory Mechanisms

TL;DR: These structure-function correlations confirm the hypothesis that transition to HF occurs by fibrosis and myocyte degeneration partially compensated by hypertrophy involving DNA synthesis and transcription.
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Tissue Engineering of a Differentiated Cardiac Muscle Construct

TL;DR: It is demonstrated that cardiac myocytes from neonatal rats, when mixed with collagen I and matrix factors, cast in circular molds, and subjected to phasic mechanical stretch, reconstitute ring-shaped EHTs that display important hallmarks of differentiated myocardium.
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Acquisition of the contractile phenotype by murine arterial smooth muscle cells depends on the Mir143/145 gene cluster

TL;DR: It is demonstrated that the mouse miR-143/145 cluster, expression of which is confined to SMCs during development, is required for VSMC acquisition of the contractile phenotype and manipulated expression may offer a new approach for influencing vascular repair and attenuating arteriosclerosis pathogenesis.
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Bone Marrow-Derived Cells Do Not Incorporate Into the Adult Growing Vasculature

TL;DR: The findings suggest that in the adult organism, bone marrow-Derived cells do not promote vascular growth by incorporating into vessel walls but may function as supporting cells.
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Sirt7 Increases Stress Resistance of Cardiomyocytes and Prevents Apoptosis and Inflammatory Cardiomyopathy in Mice

TL;DR: It is proposed that enhanced activation of p53 by lack of Sirt7-mediated deacetylation contributes to the heart phenotype of SIRT7 mutant mice, suggesting a critical role of Sirts in the regulation of stress responses and cell death in the heart.