Neurosurgical Department, PLA Navy General Hospital, Beijing, China.
Br J Pharmacol. 2012 Oct;167(4):699-719. doi: 10.1111/j.1476-5381.2012.02025.x.
Traumatic brain injury (TBI) is a major health and socioeconomic problem throughout the world. It is a complicated pathological process that consists of primary insults and a secondary insult characterized by a set of biochemical cascades. The imbalance between a higher energy demand for repair of cell damage and decreased energy production led by mitochondrial dysfunction aggravates cell damage. At the cellular level, the main cause of the secondary deleterious cascades is cell damage that is centred in the mitochondria. Excitotoxicity, Ca(2+) overload, reactive oxygen species (ROS), Bcl-2 family, caspases and apoptosis inducing factor (AIF) are the main participants in mitochondria-centred cell damage following TBI. Some preclinical and clinical results of mitochondria-targeted therapy show promise. Mitochondria- targeted multipotential therapeutic strategies offer new hope for the successful treatment of TBI and other acute brain injuries.
创伤性脑损伤(TBI)是全球范围内的一个主要健康和社会经济问题。它是一个复杂的病理过程,由原发性损伤和以一系列生化级联反应为特征的继发性损伤组成。线粒体功能障碍导致的细胞损伤修复的高能量需求与能量产生减少之间的失衡,加剧了细胞损伤。在细胞水平上,继发性有害级联反应的主要原因是集中在线粒体的细胞损伤。兴奋性毒性、Ca(2+)超载、活性氧(ROS)、Bcl-2 家族、半胱天冬酶和凋亡诱导因子(AIF)是 TBI 后以线粒体为中心的细胞损伤的主要参与者。一些针对线粒体的治疗的临床前和临床结果显示出希望。针对线粒体的多潜能治疗策略为成功治疗 TBI 和其他急性脑损伤提供了新的希望。