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unctional abnormalities of cardiac troponin caused by either mutations or auto-antibodies can induce dilated cardiomyopathy (DCM),1,2 which is characterized by left ventricular enlargement and systolic dysfunction resulting from a reduction in the myocardial force of contraction. DCM causes congestive heart failure, which can be treated with diuretics, angiotensin-converting enzyme inhibitors (or angiotensin type-I receptor blockers), β-adrenergic blockers, and most aggressively in unresponsive patients with cardiac transplantation. However, the prognosis of DCM is still poor, so there is a need for new therapeutic approaches.

Zebrafish With Antisense-Knockdown of Cardiac Troponin C as a Model of Hereditary Dilated Cardiomyopathy