Mitochondria as a therapeutic target in neurodegeneration caused by hypoxia and ischemia during the perinatal period

Perinatal hypoxia, also known as neonatal hypoxia-ischemia (HI), can pose a significant threat to the life and health of newborns, leading to hypoxic-ischemic encephalopathy (HIE) and numerous organ dysfunctions, including the nervous system. Mitochondria, which are key organelles in maintaining cellular homeostasis, adenosine triphosphate (ATP) production, regulation of apoptosis, and the cell's response to oxidative stress, appear to be particularly vulnerable to hypoxic damage. In the course of HIE, a number of mitochondrial functions may be impaired, including inhibition of the respiratory chain, increased production of reactive oxygen species (ROS), loss of mitochondrial membrane potential, or activation of apoptotic pathways. As a result of HI, mitochondrial dynamics related to the processes of mitochondrial fusion, division, and autophagy are also changed, which contributes to exacerbating neuralcell damage. Because of the significant role of mitochondria in the pathophysiology of HIE, they represent a promising therapeutic target. This article presents the current state of knowledge on mitochondrial damage mechanisms in HI and discusses potential therapeutic strategies, such as modulators of mitochondrial dynamics, antioxidant compounds, or inhibitors of specific mitochondrial pathways. A better understanding of these mechanisms may contribute to the development of more effective treatments for neurodegeneration associated with perinatal hypoxia.