Pieczenik Steve R, Neustadt John
Exp Mol Pathol. 2007 Aug;83(1):84-92. doi: 10.1016/j.yexmp.2006.09.008. Epub 2007 Jan 18.
Since the first mitochondrial dysfunction was described in the 1960s, the medicine has advanced in its understanding the role mitochondria play in health, disease, and aging. A wide range of seemingly unrelated disorders, such as schizophrenia, bipolar disease, dementia, Alzheimer's disease, epilepsy, migraine headaches, strokes, neuropathic pain, Parkinson's disease, ataxia, transient ischemic attack, cardiomyopathy, coronary artery disease, chronic fatigue syndrome, fibromyalgia, retinitis pigmentosa, diabetes, hepatitis C, and primary biliary cirrhosis, have underlying pathophysiological mechanisms in common, namely reactive oxygen species (ROS) production, the accumulation of mitochondrial DNA (mtDNA) damage, resulting in mitochondrial dysfunction. Antioxidant therapies hold promise for improving mitochondrial performance. Physicians seeking systematic treatments for their patients might consider testing urinary organic acids to determine how best to treat them. If in the next 50 years advances in mitochondrial treatments match the immense increase in knowledge about mitochondrial function that has occurred in the last 50 years, mitochondrial diseases and dysfunction will largely be a medical triumph.
自20世纪60年代首次描述线粒体功能障碍以来,医学在理解线粒体在健康、疾病和衰老中所起的作用方面取得了进展。一系列看似不相关的疾病,如精神分裂症、双相情感障碍、痴呆症、阿尔茨海默病、癫痫、偏头痛、中风、神经性疼痛、帕金森病、共济失调、短暂性脑缺血发作、心肌病、冠状动脉疾病、慢性疲劳综合征、纤维肌痛、色素性视网膜炎、糖尿病、丙型肝炎和原发性胆汁性肝硬化,都有共同的潜在病理生理机制,即活性氧(ROS)产生、线粒体DNA(mtDNA)损伤积累,导致线粒体功能障碍。抗氧化疗法有望改善线粒体性能。寻求为患者进行系统治疗的医生可能会考虑检测尿有机酸,以确定如何最好地治疗他们。如果在未来50年里,线粒体治疗的进展能与过去50年里线粒体功能知识的巨大增长相匹配,线粒体疾病和功能障碍在很大程度上将成为医学上的一项成就。