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. 2020 Mar 13;52(3):380–389. doi: 10.1038/s12276-020-0399-8

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© The Author(s) 2020

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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Fig. 1 — ASM activity increases with aging. In the aged brain, ASM levels increase in ECs of the BBB. EC-derived ASM induces BBB hyperpermeability by excessive caveolae transcytosis via PP1-mediated ERM dephosphorylation. This results in extravasation of blood-derived molecules into the brain parenchyma, leading to neuronal cell death and memory impairment. Plasma ASM levels also increase with aging, and ASM is likely to promote inflammation by causing immune cell dysfunction, such as macrophage activation and dysregulation of T cell differentiation. In aged hearts, increased ASM in muscle cells induces ceramide production. Ceramide mediates a decrease in mitochondrial cardiolipin, and this reduction contributes to mitochondrial dysfunction and cardiac impairment.