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. 2019 Oct 10;10(10):766. doi: 10.1038/s41419-019-2014-2

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© The Author(s) 2019

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. 7 — In mouse yolk sac erythrocytes, deletion of HSP60 reduced mitochondrial membrane potential. In control cells, HSP60 might bind with CypD, preventing the latter from interacting with the mPTP. When HSP60 was deleted, CypD was liberated and bound to the mPTP, which thus increased the opening of the mPTP, decreased mitochondrial membrane potential, and induced more cell apoptosis. In the end, the numbers of yolk sac erythrocytes were reduced, and the mutant embryos developed anemia and died