University of L'Aquila, Department of Life, Health and Environmental Sciences, Building Delta 6, San Salvatore Hospital, Via Vetoio, Coppito 67100 L'Aquila, Italy.
Department of Internal Medicine, Mazzoni Hospital, Ascoli Piceno, Italy.
Oxid Med Cell Longev. 2022 Aug 2;2022:9530007. doi: 10.1155/2022/9530007. eCollection 2022.
Mitochondria ensure the supply of cellular energy through the production of ATP via oxidative phosphorylation. The alteration of this process, called mitochondrial dysfunction, leads to a reduction in ATP and an increase in the production of reactive oxygen species (ROS). Mitochondrial dysfunction can be caused by mitochondrial/nuclear DNA mutations, or it can be secondary to pathological conditions such as cardiovascular disease, aging, and environmental stress. The use of therapies aimed at the prevention/correction of mitochondrial dysfunction, in the context of the specific treatment of cardiovascular diseases, is a topic of growing interest. In this context, the data are conflicting since preclinical studies are numerous, but there are no large randomized studies.
线粒体通过氧化磷酸化产生 ATP 来确保细胞能量的供应。这个过程的改变,即线粒体功能障碍,会导致 ATP 的减少和活性氧(ROS)的产生增加。线粒体功能障碍可能是由线粒体/核 DNA 突变引起的,也可能是心血管疾病、衰老和环境压力等病理状况的继发原因。在心血管疾病的具体治疗中,使用旨在预防/纠正线粒体功能障碍的治疗方法是一个日益受到关注的话题。在这方面,数据存在争议,因为有大量的临床前研究,但没有大型随机研究。