Astrocytic mitochondrial frataxin—A promising target for ischemic brain injury. (22nd December 2022)

• Record Type: Journal Article
• Authors: Hazra, Rimi; Novelli, Enrico M.; Hu, Xiaoming
• Is Part Of: CNS neuroscience & therapeutics. Volume 29:Number 3(2023)
• Page Start: 783
• Page End: 788
• Publication Date: 2022-12-22
• Subjects: astrocytes -- frataxin -- ischemia -- mitochondria; Neuropharmacology -- Periodicals; Central nervous system -- Diseases -- Effect of drugs on -- Periodicals; 612.8
• DOI: 10.1111/cns.14068
• Languages: English
• ISSNs: 1755-5930

Abstract

Abstract: In the ischemic brain, hypoxia leads to mitochondrial dysfunction, insufficient energy production, and astrocyte activation. Yet, most studies investigating mitochondrial dysfunction in cerebral ischemia have focused exclusively on neurons. This review will highlight the importance of the morphological, molecular, and functional heterogeneity of astrocytes in their role in brain injuries and explore how activated astrocytes exhibit calcium imbalance, reactive oxygen species overproduction, and apoptosis. In addition, special focus will be given to the role of the mitochondrial protein frataxin in activated astrocytes during ischemia and its putative role in the pharmacological management of cerebral ischemia. Abstract : Astrocytes interconnect cerebral microvessels with neurons. Mitochondrial function within the astrocytes regulates neuronal response during cerebrovascular ischemia. Astrocytic calcium influx may reduce frataxin (FXN) expression, thereby contributing to mitochondrial dysfunction. Targeted induction of astrocytic FXN may be an attractive therapeutic strategy for ischemic brain injury.