Modeling of lamin A/C mutation premature cardiac aging using patient‐specific induced pluripotent stem cells.

Intriguingly, the application of U0126 and selumetinib, AZD6244 (an anti-cancer drug in phase I-II clinical trial) to block MEK1 pathway in LMNA R225X/WT and LMNA Framshift/WT iPSC-CMs and shRNA treated control iPSC-CMs showed a trend that attenuated or even completely abolished the apoptotic effects of field electric stimulation on these lamin-deficient cardiomyocytes as seen in the dermal fibroblast (Figure 3 and 6 ) whereas 10 μM of U0126 significantly rescued the rate of apoptosis mediated by electrical stress (11.2 ± 0.8% vs. 4.4 ± 1.4%; n=3, P<0.05 ).

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