Background. Cardiovascular diseases, especially in association with arrhythmias, remain a prevailing cause of death worldwide. Arrhythmia related to imbalanced Ca2+ homeostasis is triggered by aberrant spontaneous diastolic Ca2+ leak from sarcoplasmic reticulum through cardiac ryanodine receptor-Ca2+ release channel (RyR2). Voltage-dependent anion channel 2 (VDAC2) is the only mammalian specific isoform also carrying a specific cardiac function.Objectives. Description of VDAC2-mediated regulation of Ca2+ concentration in cardiomyocytes. Methods. Literature sources were mined in the MedLine/PubMed and eLibrary databases with keywords “heart AND calcium”, “heart AND VDAC2”, with a subsequent analysis.Results. From 36 English-language sources, 5 were included in the review. We summarise that potentiated VDAC2 promotes mitochondrial transport of Ca2+ ions, and suppression of the channel leads to Ca2+ imbalances. Efsevin renders the channel more cation-selective and downregulates Ca2+ concentration in diastole.Conclusion. VDAC2 comprises a potential drug target in therapy for severe arrhythmias. Efsevin is a promising agent for correcting abnormal Ca2+ transport in cardiomyocytes as an accelerator of mitochondrial Ca2+ uptake.