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. 2020 Jul 24;5:119. doi: 10.1038/s41392-020-0171-5

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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. 9 — Melatonin protects against AD-associated heart dysfunction through ALDH2 and cGAS-STING-TBK1 signaling. AD is associated with decreased melatonin levels, which leads to suppressed ALDH2 activity. Impaired activity of the mitochondrial protein ALDH2 results in damage to mitochondrial integrity, causing mtDNA to be released into the cytosol. A large amount of mtDNA depletes cGAS-STING-TBK1 signaling, leading to suppressed levels of autophagy and mitophagy. These responses further impair clearance of Aβ and mitochondria, ultimately resulting in heart dysfunction. Melatonin supplementation protects heart function in AD by boosting ALDH2 activity through PKCε, thus restoring mitochondrial integrity, cGAS-STING-TBK1 signaling, and autophagy and mitophagy levels