Zebrafish Heart as a Model to Elucidate the Mechanisms of Sudden Cardiac Death

Abstract

The heart of zebrafish has been used as a simple, low-cost model to study development, structure and function of the heart from early to late stages of life. Also, it has been established as a model to study different cardiac pathologies generated through different methods. Cardiac pathologies include from functional disorders such as arrhythmia, to structural disorders such as hypertrophic heart disease; in many of them, genetic and molecular aspects have been associated. Noteworthy, some of these genetic and molecular factors have been invoked as causes of sudden cardiac death in humans. This adverse outcome is common in many cardiovascular pathologies and can occur at any age. Unfortunately, etiology and physiopathology of sudden cardiac death are unclear, so extensive research in this area is required. This mini-review highlight three related points: First, the relevance of sudden cardiac death in humans. Second, advances in knowledge of the development, function and pathologies in the zebrafish heart model. Finally, the possibility of using the zebrafish model for the study of sudden cardiac. For this review, a literature search was performed using the PubMed database and the search engine Google Scholar: the words sudden cardiac death, zebrafish, arrhythmias, cardiomyopathies were combined for this search.

Automated Patch-Clamp and Induced Pluripotent Stem Cell-Derived Cardiomyocytes: A Synergistic Approach in the Study of Brugada Syndrome

“…The electrophysiology of the zebrafish heart is similar to that of humans, with an ECG that closely resembles the human one, and a ventricular action potential (AP) exhibiting the plateau phase seen in humans but absent in mice, as well as a robust IK 1 current for sustaining resting membrane potential. The functionality of the zebrafish heart has been assessed using conventional patch-clamp techniques, as well as ex vivo and in vivo recordings of whole zebrafish hearts or isolated atrial and ventricular cardiomyocytes [ 40 ]. A BrS model in zebrafish was generated by knocking out the glutathione S-transferase mu 3 ( GSTM3 ) gene, a genetic modifier of the BrS phenotype [ 41 ].…”