Mechanistic study of optic atrophy 1 in ischemia-reperfusion disease.

Mitochondria consist of the inner mitochondrial membrane and the outer mitochondrial membrane, which maintain mitochondrial homeostasis through continuous fission and fusion to ensure a healthy mitochondrial network and thus regulate normal cellular function, namely mitochondrial dynamics. The imbalance between mitochondrial fusion and fission results in abnormal mitochondrial structure and eventually mitochondrial dysfunction, which is involved in the pathological process of ischemia-reperfusion injury (IRI). Optic atrophy 1 (OPA1) is a key protein that regulates mitochondrial inner membrane fusion and ensures normal mitochondrial function by balancing mitochondrial dynamics, participating in various processes such as mitochondrial fusion, oxidative stress, and apoptosis. Ischemia-induced changes in mitochondrial dynamics may be a key factor in limiting the recanalization time window and exacerbating reperfusion injury, and the mechanisms of these changes deserve further attention. Therefore, targeting OPA1-related mitochondrial fusions, thereby balancing mitochondrial dynamics and improving mitochondrial dysfunction, is a promising therapeutic strategy for ischemia-reperfusion diseases. This review will elaborate on the structure and function of OPA1 and the role of OPA1 in IRI to provide promising therapeutic targets for the treatment of ischemia-reperfusion diseases.