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. 2022 Nov 4;13:6634. doi: 10.1038/s41467-022-34316-3

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© The Author(s) 2022

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 — (Top) Mtfp1 deletion in cardiomyocytes occurs at birth (cMKO) and sensitizes cardiac myocytes to mitochondrial permeability transition pore (mPTP) opening, cell death and increases mitochondria uncoupling of the inner membrane. At the adult age of 8–10 weeks heart of cMKO mice have normal structure and function but undergoes to the development of a progressive dilated cardiomyopathy (DCM) at 18 weeks which progresses to severe heart failure and middle-aged death by 34 weeks. At onset of DCM, cMKO mice exhibit increased cardiac cell death, reduced mitochondrial respiration, and induction of a sterile inflammatory response. (Bottom) Coupled respiration and mPTP closure is maintained by MTFP1. Genetic deletion of Mtfp1 promotes the ANT-dependent uncoupling of mitochondrial respiration and opening of the mPTP, sensitizing cells to programmed cell death. Figure created with BioRender.