Neuroscience Research Center, Department of Neurosurgery, Poursina Hospital,School of Medicine,Guilan University of Medical Sciences,Rasht,Iran.
Department of Neurology,University of Minnesota,Minneapolis, MN,USA.
Expert Rev Mol Med. 2017 Apr 5;19:e5. doi: 10.1017/erm.2017.5.
Ischaemic heart disease and stroke are vascular events with serious health consequences worldwide. Recent genetic and epigenetic techniques have revealed many genetic determinants of these vascular events and simplified the approaches to research focused on ischaemic heart disease and stroke. The pathogenetic mechanisms of ischaemic heart disease and stroke are complex, with mitochondrial involvement (partially or entirely) recently gaining substantial support. Not only can mitochondrial reactive oxygen species give rise to ischaemic heart disease and stroke by production of oxidised low-density lipoprotein and induction of apoptosis, but the impact on pericytes contributes directly to the pathogenesis. Over the past two decades, publications implicate the causative role of nuclear genes in the development of ischaemic heart disease and stroke, in contrast to the potential role of mitochondrial DNA (mtDNA) in the pathophysiology of the disorders, which is much less understood, although recent studies do demonstrate that the involvement of mitochondria and mtDNA in the development of ischaemic heart disease and stroke is likely to be larger than originally thought, with the novel discovery of links among mitochondria, mtDNA and vascular events. Here we explore the molecular events and mtDNA alterations in relation to the role of mitochondria in ischaemic heart disease and stroke.
缺血性心脏病和中风是具有严重健康后果的血管事件。最近的遗传和表观遗传技术揭示了这些血管事件的许多遗传决定因素，并简化了专注于缺血性心脏病和中风的研究方法。缺血性心脏病和中风的发病机制很复杂，线粒体的参与（部分或全部）最近得到了大量支持。线粒体活性氧不仅可以通过产生氧化低密度脂蛋白和诱导细胞凋亡而导致缺血性心脏病和中风，而且对周细胞的影响也直接导致发病机制。在过去的二十年中，出版物表明核基因在缺血性心脏病和中风的发展中起因果作用，而线粒体 DNA（mtDNA）在这些疾病的病理生理学中的潜在作用则知之甚少，尽管最近的研究确实表明，线粒体和 mtDNA 参与缺血性心脏病和中风的发展的可能性比最初想象的要大，新发现线粒体、mtDNA 和血管事件之间存在联系。在这里，我们探讨了与线粒体在缺血性心脏病和中风中的作用有关的分子事件和 mtDNA 改变。
