线粒体由线粒体内膜和线粒体外膜组成，通过持续的裂变和融合维持线粒体稳态，以确保健康的线粒体网络，从而调节正常的细胞功能，即线粒体动力学。线粒体融合和分裂之间的失衡导致线粒体结构异常，最终导致线粒体功能障碍。参与了缺血再灌注损伤(IRI)的病理过程。视神经萎缩1（OPA1）是调节线粒体内膜融合并通过平衡线粒体动力学来确保正常线粒体功能的关键蛋白，参与各种过程，如线粒体融合，氧化应激，和凋亡。缺血诱导的线粒体动力学变化可能是限制再通时间窗和加重再灌注损伤的关键因素。这些变化的机制值得进一步关注。因此,靶向OPA1相关的线粒体融合，从而平衡线粒体动力学并改善线粒体功能障碍，是缺血再灌注疾病的一种有前途的治疗策略。本文将对OPA1的结构和功能以及OPA1在IRI中的作用进行综述，为缺血再灌注疾病的治疗提供有希望的治疗靶点。
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.
