{"title":"Commentary: Can astrocytic mitochondria therapy be used as antioxidant conditioning to protect neurons?","authors":"Kazuhide Hayakawa","doi":"","DOIUrl":null,"url":null,"abstract":"<p><p>In the context of central nervous system (CNS) disease, oxidative stress may cause progression of cell death and neuroinflammation. Therefore, restoring mitochondrial antioxidant ability within cells is a major therapeutic strategy in many CNS disorders. A recent study uncovers a novel mechanism of astrocytic mitochondria being neuroprotective after intracerebral hemorrhage in mice. In their work, systemic administration of mitochondria obtained from astrocytes restores neuronal antioxidant defense, prevents neuronal death while promoting neurite outgrowth, indicating that extracellular mitochondria may play key roles in mediating beneficial non-cell autonomous effects. Given that mitochondria are also responsible for tolerance to stress and injury, is it possible that exogenous mitochondria signals may regulate cellular conditioning by boosting antioxidant ability? Further studies are warranted to build on these emerging findings in the pursuit of conditioning therapies mediated by mitochondrial transplantation in CNS injury and disease.</p>","PeriodicalId":72686,"journal":{"name":"Conditioning medicine","volume":"5 6","pages":"192-195"},"PeriodicalIF":0.0000,"publicationDate":"2022-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10688760/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Conditioning medicine","FirstCategoryId":"1085","ListUrlMain":"","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
In the context of central nervous system (CNS) disease, oxidative stress may cause progression of cell death and neuroinflammation. Therefore, restoring mitochondrial antioxidant ability within cells is a major therapeutic strategy in many CNS disorders. A recent study uncovers a novel mechanism of astrocytic mitochondria being neuroprotective after intracerebral hemorrhage in mice. In their work, systemic administration of mitochondria obtained from astrocytes restores neuronal antioxidant defense, prevents neuronal death while promoting neurite outgrowth, indicating that extracellular mitochondria may play key roles in mediating beneficial non-cell autonomous effects. Given that mitochondria are also responsible for tolerance to stress and injury, is it possible that exogenous mitochondria signals may regulate cellular conditioning by boosting antioxidant ability? Further studies are warranted to build on these emerging findings in the pursuit of conditioning therapies mediated by mitochondrial transplantation in CNS injury and disease.