Sometimes less is more: inhibitory infrared light during early reperfusion calms hyperactive mitochondria and suppresses reperfusion injury
- 6 September 2022
- journal article
- research article
- Published by Portland Press Ltd. in Biochemical Society Transactions
- Vol. 50 (5), 1377-1388
- https://doi.org/10.1042/bst20220446
Abstract
Ischemic stroke affects over 77 million people annually around the globe. Due to the blockage of a blood vessel caused by a stroke, brain tissue becomes ischemic. While prompt restoration of blood flow is necessary to save brain tissue, it also causes reperfusion injury. Mitochondria play a crucial role in early ischemia-reperfusion injury due to the generation of reactive oxygen species (ROS). During ischemia, mitochondria sense energy depletion and futilely attempt to up-regulate energy production. When reperfusion occurs, mitochondria become hyperactive and produce large amounts of ROS which damages neuronal tissue. This ROS burst damages mitochondria and the cell, which results in an eventual decrease in mitochondrial activity and pushes the fate of the cell toward death. This review covers the relationship between the mitochondrial membrane potential (ΔΨm) and ROS production. We also discuss physiological mechanisms that couple mitochondrial energy production to cellular energy demand, focusing on serine 47 dephosphorylation of cytochrome c (Cytc) in the brain during ischemia, which contributes to ischemia-reperfusion injury. Finally, we discuss the use of near infrared light (IRL) to treat stroke. IRL can both stimulate or inhibit mitochondrial activity depending on the wavelength. We emphasize that the use of the correct wavelength is crucial for outcome: inhibitory IRL, applied early during reperfusion, can prevent the ROS burst from occurring, thus preserving neurological tissue.Keywords
This publication has 100 references indexed in Scilit:
- Transcranial Red and Near Infrared Light Transmission in a Cadaveric ModelPLOS ONE, 2012
- Regulation of mitochondrial respiration and apoptosis through cell signaling: Cytochrome c oxidase and cytochrome c in ischemia/reperfusion injury and inflammationBiochimica et Biophysica Acta (BBA) - Bioenergetics, 2012
- ER-Mitochondria Crosstalk during Cerebral Ischemia: Molecular Chaperones and ER-Mitochondrial Calcium TransferInternational Journal of Cell Biology, 2012
- Focal Cerebral Ischemia Model by Endovascular Suture Occlusion of the Middle Cerebral Artery in the RatJournal of Visualized Experiments, 2011
- Phosphoproteome Analysis of Functional Mitochondria Isolated from Resting Human Muscle Reveals Extensive Phosphorylation of Inner Membrane Protein Complexes and EnzymesMolecular & Cellular Proteomics, 2011
- The Binding Interface of Cytochrome c and Cytochrome c1 in the bc1 Complex: Rationalizing the Role of Key ResiduesBiophysical Journal, 2010
- Reversible Cyclosporin A-sensitive Mitochondrial Depolarization Occurs within Minutes of Stroke Onset in Mouse Somatosensory Cortex in VivoOnline Journal of Public Health Informatics, 2009
- In vivo Phosphoproteome of Human Skeletal Muscle Revealed by Phosphopeptide Enrichment and HPLC−ESI−MS/MSJournal of Proteome Research, 2009
- Membrane Potential Greatly Enhances Superoxide Generation by the Cytochrome bc1 Complex Reconstituted into Phospholipid VesiclesOnline Journal of Public Health Informatics, 2009
- How mitochondria produce reactive oxygen speciesBiochemical Journal, 2008