Mitochondria are double-membrane organelles that provide the majority of a cell's energy. Furthermore, mitochondria are involved in various cellular biological activities, including calcium signalling, reactive oxygen species production, apoptosis, cell development, and the cell cycle. Mitochondrial dysfunction is seen in various neurological conditions involving acute and chronic neural injury, including neurodegenerative diseases, hypoxia-induced brain injury, and ischemia. This review made a significant contribution to the explanation of the idea that mitochondria would both be critical targets of ischemia-induced processes, including intracellular calcium elevation and reactive oxygen species and essential sites for determining cell viability loss. As a result, it's not unexpected that attempts to prevent I/R damage have focused on mitochondria. Drugs such as vatiquinone, vitexin, dexprmipexole, baicalin, nobiletin, via promoting mitochondrial activities, can be used in future studies for protecting the brain from ischemia injury. This review summarizes mitochondrial pathways, i.e., Bad, Drp-1, JNK/caspase-3, MAPK-ERK, p53, Wnt/β-Catenin, that contribute to disease progression. We have précised the potential regulatory role of miRNA-mitochondrial dynamics in cerebral ischemic-reperfusion injury and associated molecular mechanisms; also provide insight into the potential therapies for cerebral injury-induced injuries.
Keywords: Apoptosome; Cerebral ischemia–reperfusion injury; Mitochondrial dynamics; miRNA.
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