PDF(Pubmed)
Abstract：
Cardiovascular disease is the most common cause of death worldwide and in particular, ischemic heart disease holds the most considerable position. Even if it has been deeply studied, myocardial ischemia-reperfusion injury (IRI) is still a side-effect of the clinical treatment for several heart diseases: ischemia process itself leads to temporary damage to heart tissue and obviously the recovery of blood flow is promptly required even if it worsens the ischemic injury. There is no doubt that mitochondria play a key role in pathogenesis of IRI: dysfunctions of these important organelles alter cell homeostasis and survival. It has been demonstrated that during IRI the system of mitochondrial quality control undergoes alterations with the disruption of the complex balance between the processes of mitochondrial fusion, fission, biogenesis and mitophagy. The fundamental role of mitochondria is carried out thanks to the finely regulated connection to other organelles such as plasma membrane, endoplasmic reticulum and nucleus, therefore impairments of these inter-organelle communications exacerbate IRI. This review pointed to enhance the importance of the mitochondrial network in the pathogenesis of IRI with the aim to focus on potential mitochondria-targeting therapies as new approach to control heart tissue damage after ischemia and reperfusion process.
摘要：
心血管疾病是全球最常见的死亡原因，缺血性心脏病占有最重要的地位。即使经过了深入的研究,心肌缺血再灌注损伤(IRI)仍然是临床治疗几种心脏疾病的副作用:缺血过程本身会导致心脏组织的暂时性损伤,即使缺血损伤加重,也需要及时恢复血流。毫无疑问，线粒体在IRI的发病机理中起着关键作用：这些重要细胞器的功能障碍会改变细胞的稳态和存活。已经证明，在IRI期间，线粒体质量控制系统会随着线粒体融合过程之间复杂平衡的破坏而发生变化，裂变,生物发生和线粒体自噬。线粒体的基本作用是由于与其他细胞器如质膜的精细调节连接而实现的，内质网和细胞核，因此,这些细胞器间通信的受损会加剧IRI.这篇综述指出，增强线粒体网络在IRI发病机制中的重要性，旨在关注潜在的线粒体靶向治疗作为控制缺血和再灌注过程后心脏组织损伤的新方法。
