Contractile deficits in engineered cardiac microtissues as a result of MYBPC3 deficiency and mechanical overload-Reference-Cited by-同舟云学术

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Contractile deficits in engineered cardiac microtissues as a result of MYBPC3 deficiency and mechanical overload

Published:2018-09-10 Issue:12 Volume:2 Page:955-967
ISSN:2157-846X
Container-title:Nature Biomedical Engineering
language:en
Short-container-title:Nat Biomed Eng

Author:

Ma Zhen,Huebsch Nathaniel,Koo Sangmo,Mandegar Mohammad A.,Siemons Brian,Boggess Steven,Conklin Bruce R.,Grigoropoulos Costas P.,Healy Kevin E.

Publisher

Springer Science and Business Media LLC

Subject

Computer Science Applications,Biomedical Engineering,Medicine (miscellaneous),Bioengineering,Biotechnology

Link

http://www.nature.com/articles/s41551-018-0280-4.pdf

Reference56 articles.

1. Carrier, L., Mearini, G., Stathopoulou, K. & Cuello, F. Cardiac myosin-binding protein C (MYBPC3) in cardiac pathophysiology. Gene 573, 188–197 (2015).

2. Strande, J. L. Haploinsufficiency MYBPC3 mutations: another stress induced cardiomyopathy? Let’s take a look! J. Mol. Cell. Cardiol. 79, 284–286 (2015).

3. Feric, N. T. & Radisic, M. Maturing human pluripotent stem cell-derived cardiomyocytes in human engineered cardiac tissues. Adv. Drug Deliv. Rev. 96, 110–134 (2016).

4. Mathur, A. et al. In vitro cardiac tissue models: current status and future prospects. Adv. Drug Deliv. Rev. 96, 203–213 (2016).

5. Eng, G. et al. Autonomous beating rate adaptation in human stem cell-derived cardiomyocytes. Nat. Commun. 7, 10312 (2016).

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