Figure 6.

Co‐administration of a STAT inhibitor abrogates erlotinib‐induced increase in cardiomyocyte fatty acid oxidation in vitro and impairs contractile function in vivo. A, Neonatal rat ventricular myocytes (n=4 independent experiments) were treated with vehicle, the carnitine phosphatoyl transferase inhibitor, etomoxir, or kinase inhibitors (including the STAT inhibitor, STATTIC) for 24 h, then fatty acid oxidation was assayed using ¹⁴C‐oleate. B, Cell death in NRVMs was assayed by LDH release (n=3–5 independent experiments, as indicated). C, Female FVB mice were treated with vehicle, erlotinib, and/or the STAT inhibitor WP1066 for 7 days and contractile function was assessed using conscious echocardiography. Groups for all experiments were compared using 1‐way ANOVA, *P<0.05, **P<0.01. LDH indicates lactate dehydrogenase; NRVMs, neonatal rat ventricular myocytes; NS, not significant; STAT, signal transducer and activator of transcription.