Open AccessVDAC2-mediated regulation of calcium homeostasis in cardiomyocytes (a review)
Author(s) -
N. V. Schcetinina,
A.A. Bolotskaya
Publication year - 2020
Publication title -
kubanskij naučnyj medicinskij vestnik
Language(s) - English
Resource type - Journals
eISSN - 2541-9544
pISSN - 1608-6228
DOI - 10.25207/1608-6228-2020-27-6-164-174
Subject(s) - ryanodine receptor , ryanodine receptor 2 , endoplasmic reticulum , homeostasis , calcium , mitochondrion , voltage dependent anion channel , microbiology and biotechnology , medicine , chemistry , endocrinology , diastole , calcium metabolism , pharmacology , biology , biochemistry , escherichia coli , bacterial outer membrane , gene , blood pressure
Background . Cardiovascular diseases, especially in association with arrhythmias, remain a prevailing cause of death worldwide. Arrhythmia related to imbalanced Ca 2+ homeostasis is triggered by aberrant spontaneous diastolic Ca 2+ leak from sarcoplasmic reticulum through cardiac ryanodine receptor-Ca 2+ release channel (RyR2). Voltage-dependent anion channel 2 (VDAC2) is the only mammalian specic isoform also carrying a specic cardiac function. Objectives . Description of VDAC2-mediated regulation of Ca 2+ 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 Ca 2+ ions, and suppression of the channel leads to Ca 2+ imbalances. Efsevin renders the channel more cation-selective and downregulates Ca 2+ concentration in diastole. Conclusion . VDAC2 comprises a potential drug target in therapy for severe arrhythmias. Efsevin is a promising agent for correcting abnormal Ca 2+ transport in cardiomyocytes as an accelerator of mitochondrial Ca 2+ uptake.