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. 2017 Jul 3;7:4546. doi: 10.1038/s41598-017-04874-4

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© The Author(s) 2017

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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Proposed model depicting the molecular mechanisms by which HDAC6 promotes vascular remodeling in PAH. To deal with stressful conditions, HSP90 is upregulated in PAH-PASMCs and stabilizes HDAC6. HDAC6 maintains cytosolic Ku70 in a hypoacetylated state preventing Bax translocation to mitochondria and subsequent apoptosis. This results in increased cell survival contributing to vascular remodeling and PAH progression. Conversely, HSP90 or HDAC6 inhibition increases Ku70 acetylation and Bax release promoting mitochondrial membrane depolarization and programmed cell death.