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Article Abstract
Hypoxic-ischemic brain injury (HIBI) is a prevalent global health challenge, which is characterized by high disability and mortality rates. Despite extensive research, effective therapeutic interventions that can mitigate the influences of this disease and reduce associated disability and mortality rates remain elusive. Hypoxia-ischemia-induced energy deficiency in brain tissue not only impairs neurons but also disrupts the structural and functional integrity of mitochondria. This review focuses on mitochondrial reprogramming in hypoxia-ischemia brain injury and targeting mitochondrial reprogramming as a therapeutic goal to mitigate mitochondrial damage and restore neuronal energy supply. Mitochondrial reprogramming refers to a series of adaptive changes (including changes in size, fusion, fission, transport and anchoring) that mitochondria undergo in response to changes in cellular metabolism under physiological or pathological conditions. Our systematic summary of new therapeutic directions for mitochondrial reprogramming in hypoxic-ischemic brain injury models, particularly the mechanism of action of MitoQ, Ferrostatin-1analogue (UAMC-3203), to protect damaged neurons, points to a new therapeutic strategy for neonatal hypoxic-ischemic brain injury disorders.
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| http://dx.doi.org/10.1016/j.neuroscience.2025.07.043 | DOI Listing |
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