142 Chapter 6 more cost- and technology-intensive, thus probably less promising for high-throughput applications and screens. Finally, we confirmed the applicability of MM iPSC-CM to model hypoxic damage by validating the protective effects of the necroptosis inhibitor Nec-1, in contrast to conventional, non-MM iPSC-CM culture conditions. In summary, we have shown that MM iPSC-CMs display increased sensitivity to hypoxic injury, which is more reminiscent of adult CMs and therefore represent an improved model for human ischemic heart disease in vitro. ACKNOWLEDGEMENTS The authors would like to acknowledge Joseph Wu (Stanford Medicine, USA) for providing the CVI-273 hiPS cell line. We thank Maike Kreutzenbeck and Rebecca Dieterich (Šarić group, University of Cologne) for their technical support with the generation and characterisation of the NP0141-31B / UKKi032-C iPSC line. M.C.P. and K.N. were supported by a Netherlands Cardiovascular Research Initiative (CVON) grant (REMAIN 2014B27) and a Health~Holland LSH-TKI grant (DELICATE LSHM19086). M.M. is supported by the National Institutes Health (5P01HL141084 and 1R01HL152055) and Foundation Leducq (CUREPLaN). T.Š. was supported by the Innovative Medicine Initiative Joint Undertaking (IMI-JU) funded by the European Commission and the European Federation of Pharmaceutical Industries and Associations (EFPIA, grant agreement No. 115582, “European Bank for induced Pluripotent Stem Cells, EBiSC). J.P.G.S and R.G.C.M were supported by the PLN foundation, J.P.G.S and A.v.M. were supported by Horizon2020 ERC-2016-COG-EVICARE (grant number 725229) and BRAVE (grant number 874827). Disclosure of Potential Conflicts of Interest The authors disclose no conflicts of interest.
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