NRG1 and dilated cardiomyopathy: TZM has been reported to potentiate cardiomyocyte toxicity through a “dual-hit” mechanism, which includes alterations in antiapoptotic signalling pathways in cardiomyocytes, inhibition of the neuregulin-1 survival signaling pathway, and angiotensin II-induced activation of NADPH oxidase, with the ability to further increase reactive oxygen species production, ultimately resulting in dilated cardiomyopathy [78, 79].