Trastuzumab-induced cardiac dysfunction: A 'dual-hit'.

摘要: Trastuzumab (Trz) is a monoclonal antibody against the human epidermal growth factor receptor 2 that found to be overexpressed in 25% 30% of breast cancer patients. In spite therapeutic benefits Trz, cardiotoxic side effects are still an issue. This effect potentiated particularly when Trz administered following doxorubicin (DOX) treatment. Among various mechanisms may account for DOX and Trz-induced cardiotoxicity, role oxidative stress has gained significant support. The present review discusses evidence supporting hypothesis comes from multiple sources through increase production reactive oxygen species and/or decrease antioxidant defense systems. adjuvant use can potentiate cardiomyocyte damage ‘dual-hit’ mechanism, which includes inhibition neuregulin-1 survival signalling pathway angiotensin II-induced activation NADPH oxidase, with ability further production. Preventive therapies DOX- cardiac dysfunction have eluded investigators, but include prophylactic angiotensin-converting enzyme inhibitors, beta-blockers antioxidants. Thus, better understanding leading this characteristic drug-induced cardiomyopathy, as well potential cardioprotective strategies required.