Ryan J. Mailloux

TL;DR: These findings are consistent with the notion that UCPs 2 and 3 are acutely activated by ROS, which then directly modulate the glutathionylation status of the UCP to decrease ROS emission and participate in cell signaling mechanisms.

TL;DR: A novel way in which OPA1 senses energy substrate availability is proposed, which modulates its function in the regulation of mitochondrial architecture in a SLC25A protein‐dependent manner.

TL;DR: In conclusion, the increased production of KG mediated by NADP-dependent isocitrate dehydrogenase (NADP-ICDH) and its decreased utilization via the TCA cycle confer a unique strategy to modulate the cellular redox environment.

TL;DR: This work provides the first comprehensive review on how redox signals mediated through cysteine oxidation, namely S-oxidation, S-glutathionylation, and S-nitrosylation, regulate key mitochondrial functions including nutrient oxidation, oxidative phosphorylation, ROS production, mitochondrial permeability transition (MPT), apoptosis, and mitochondrial fission and fusion.

TL;DR: The results indicate that differentiating human primary myoblasts in GAL enhances aerobic metabolism and may be useful in further studies of the molecular mechanisms of mitochondrial dysfunction.