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Modeling Human Cardiac Hypertrophy in Stem Cell-Derived Cardiomyocytes

Ovchinnikova, E., Hoes, M., Ustyantsev, K., Bomer, N., de Jong, T. V., van der Mei, H., Berezikov, E. & van der Meer, P., 13-Mar-2018, In : Stem Cell Reports. 10, 3, p. 794–807 14 p.

Research output: Contribution to journalArticleAcademicpeer-review

Cardiac hypertrophy accompanies many forms of cardiovascular diseases. The mechanisms behind the development and regulation of cardiac hypertrophy in the human setting are poorly understood, which can be partially attributed to the lack of a human cardiomyocyte-based preclinical test system recapitulating features of diseased myocardium. The objective of our study is to determine whether human embryonic stem cell-derived cardiomyocytes (hESC-CMs) subjected to mechanical stretch can be used as an adequate in vitro model for studying molecular mechanisms of cardiac hypertrophy. We show that hESC-CMs subjected to cyclic stretch, which mimics mechanical overload, exhibit essential features of a hypertrophic state on structural, functional, and gene expression levels. The presented hESC-CM stretch approach provides insight into molecular mechanisms behind mechanotransduction and cardiac hypertrophy and lays groundwork for the development of pharmacological approaches as well as for discovering potential circulating biomarkers of cardiac dysfunction. In this article, Berezikov, van der Meer, and colleagues used stem cell-derived cardiomyocytes to model human cardiac hypertrophy. Their approach provides novel insights into molecular mechanisms behind mechanotransduction and cardiac hypertrophy and lays groundwork for the development of new pharmacological approaches as well as for discovering new potential circulating biomarkers of cardiac dysfunction.

Original languageEnglish
Pages (from-to)794–807
Number of pages14
JournalStem Cell Reports
Volume10
Issue number3
Publication statusPublished - 13-Mar-2018

    Keywords

  • Cardiomyocytes stretch response, Human cardiomyocytes, Hypertrophy, in vitro disease modeling, Mechanotransduction, Stem cells, GROWTH, APOPTOSIS, PRESERVED EJECTION FRACTION, HEART-FAILURE, FIBROBLAST ACTIVATION, TRANSCRIPTION FACTOR, THERAPEUTIC TARGET, VOLUME OVERLOAD, GENE-EXPRESSION, PROTEIN

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