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. 2018 Apr 25;8:6533. doi: 10.1038/s41598-018-24908-9

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© The Author(s) 2018

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Overview of calcium pathways assessed in this study. Mechanisms of Ca²⁺ transport are given in bold, the respective interfering substance in italics. Intracellular pathways are denoted in green, transport across the cell membrane in blue and non-physiological mechanisms (i.e. cell perforation) in red. In the case of lidocaine, the substance does not interfere directly with the VDCCs but with voltage-dependent sodium channels, which would in turn activate the VDCCs. Calcium ions (white spheres) can be transported to the cytoplasm from the outside medium or intracellular sources, using both physiological and pathophysiological pathways. The MPT pore is closed under physiological conditions. Membrane channels of the ER can be triggered via a positive feedback loop which induces calcium-induced calcium release. TRP, transient receptor potential channels; VDCCs, voltage dependent calcium channels; IP₃R, inositol trisphosphate receptors; RyR, ryanodine receptors; NCLX, mitochondrial sodium calcium exchanger; ER, endoplasmic reticulum. Figure elements from Servier Medical Art (http://smart.servier.com).