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. 2017 Dec 1;6(1):182–191. doi: 10.1089/biores.2017.0023

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© Kathryn Taggart et al. 2017; Published by Mary Ann Liebert, Inc.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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FIG. 3. — Increased mitochondrial stress and activation of intrinsic apoptotic signaling in PDK4 deficient cells. (A) Increased mitochondrial toxicity was observed in starved PDK4^del/del fibroblasts (**p < 0.01). The toxicity level decreased to unstarved levels following administration of AAV-PDK4 (***p < 0.001). (B) An increase in ATP production was observed in starved PDK4^wt/del and PDK4^del/del fibroblasts. ATP levels decreased following administration of AAV-PDK4 (***p < 0.001). (C) An increase in ROS production was observed in starved PDK4^wt/del and PDK4^del/del fibroblasts (**p < 0.01). ROS levels decreased following administration of AAV-PDK4 (***p < 0.001). (D) An increase in caspase-9 activity levels was observed in starved PDK4^wt/del and PDK4^del/del fibroblasts (**p < 0.01). Caspase-9 levels decreased following the administration of AAV-PDK4 (***p < 0.001). ROS, reactive oxygen species.