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. 2023 May 15;13:7855. doi: 10.1038/s41598-023-34789-2

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© The Author(s) 2023

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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/.

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A summarized scheme of how HypoMg causes seizures and death. Upregulated TRPM7 kinase function by HypoMg induces seizures and death in mice, accompanied with kinase phosphorylation (p-PKCα/δ and p-Pyk2), RyR2 phosphorylation (p-RyR2), MCU overexpression, inflammation and oxidative stress in the brain. Inhibition of TRPM7 kinase by a K1646R mutation prevents all these HypoMg-induced changes. HypoMg hypomagnesemia, TRPM7 transient receptor potential cation channel subfamily M 7, p-PKC phosphorylated protein kinase C, p-RyR2 phosphorylated ryanodine receptor 2, MCU mitochondrial calcium uniporter, p-Pyk2 phosphorylated protein tyrosine kinase 2; ↑, increased; Ͱ, inhibition.