About This ProjectThis project was an invited review that is currently under minor revision at Frontiers Cellular and Developmental Biology. The review focuses on redox signaling in control of mitochondrial energy metabolism and how deregulation of these key signaling cascades in mitochondria leads to development of diseases like heart disease and obesity.
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What is the context of this research?
Invited review currently under minor revision at Frontiers Cellular and Developmental Biology, special issue on energy metabolism and diseases. Review focuses on the role of S-glutathionylation in the control of mitochondrial function. S-glutathionylation is a redox sensitive modification involving the formation of a disulfide bridge between the antioxidant glutathione and a protein cysteine thiol. More importantly mitochondria are sensitive towards redox signaling via S-glutathionylation. This invited review sheds light on the importance of redox signaling in mitochondria and how these pathways are deregulated in various disease states.
What is the significance of this project?
Redox signaling has emerged over the years as a key signaling pathway that cross communications with other signaling pathways (e.g. phosphorylation) to modulate cellular function. It is now well known that S-glutathionylation plays a part in modulating transcription and translation as well as calcium homeostasis and muscle contraction. Over the past decade it has also become clear that mitochondria are important sites for S-glutathionylation signaling as well. Mitochondria harbor a number of enzymes involved in oxidative phosphorylation that can be modulated by S-glutathionylation. The present review focuses on how S-glutathionylation plays a central role in modulating mitochondrial function and explains the importance of this signaling cascade in maintenance of health.
What are the goals of the project?
The immediate goal of this project is to illustrate the emerging importance of redox signaling through S-glutathionylation reactions in the modulation of mitochondrial function. Indeed, the concept of redox signaling in mitochondria through S-glutathionylation reactions is novel and is now considered a key pathway in controlling mitochondrial energy metabolism, dynamics, and induction of cell death in response to changes in redox environment. This invited review pulls together all the information on the subject in an attempt to synthesize new concepts on redox signaling in mitochondria in health and disease
Publication fees - 1300 CAD. Publication fees are required for the production of the article. This includes formatting, image rendering, and publication of article in journal issues. As Frontiers is an open access journal, meaning anyone can access the article for free, additional fees are added for publication.
Meet the Team
Team BioI have been working in mitochondrial metabolism for a decade focusing on NADPH homeostasis, antioxidant defense, control of ROS production by mitochondria and the impact ROS has on Krebs cycle enzymes and respiratory complexes. Most of the work I have conducted has been in the contact of human health and disease, in particular dysfunctional mitochondrial metabolism and perturbations in maintenance of redox homeostasis in various human diseases. Over the past five years, I have become very interested in redox signaling, mostly through S-glutathionylation and how S-glutathionylation reactions can control mitochondrial function. I have published over ten articles on the subject including original research communications and reviews. These articles have been published in prestigious medium and high impact journals. The present article I wish to fund is an invited review for Frontiers, an open access journal that is part of the Nature Publishing Group.
- $1,400Total Donations
- $127.27Average Donation