Astrocytic mitochondrial frataxin-A promising target for ischemic brain injury

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.

Automated summary

In ischemic brain, lack of oxygen causes mitochondrial dysfunction, limited energy production, and activation of astrocytes. However, most studies on mitochondrial dysfunction in cerebral ischemia have focused on neurons. This review emphasizes the importance of the diverse morphology, molecules, and functions of astrocytes in their role in brain injuries, and explores how activated astrocytes exhibit calcium imbalance, excessive reactive oxygen species, and apoptosis. Additionally, it specifically focuses on the role of mitochondrial protein frataxin in activated astrocytes during ischemia and its potential role in the pharmacological management of cerebral ischemia.