The advent of epigenetics brought in a tectonic shift in the understanding of molecular basis of complex diseases like ischemic stroke (IS). Substantial scientific inquiry into the epigenetic basis of neurodegenerative diseases has bolstered the idea that altered carbon flux into central carbon metabolism and disturbed redox states govern the attendant transcriptional profiles through stochastic epigenetic changes. In view of an increasing understanding of the link between mitochondrial energy metabolism, oxidative stress and epigenetics in IS, the hitherto underappreciated 'neuroenergetics' is gaining sustained attention. Defined metabolic transitions during IS are necessarily a function of transiently altered abundance of critical metabolic substrates of Krebs cycle and other pathways viz., acetyl-CoA, citrate, 2-oxo-glutarate, succinate, fumarate, S-adenosyl methionine, β-hydroxybutyrate and cofactors (NAD+, FAD, ATP, vitamin C) in neuronal mitochondria. These changes impinge on the cellular transcriptome by regulating the activity of several chromatin modifying enzymes that bring about epigenomic transition through alteration in DNA methylation and histone post translational modifications. This triggers downstream signaling cascades that circumstantially evoke adaptive and cell death responses during IS. Indeed, they also prevail on the functionality of neuronal network, brain plasticity and neurogenesis during post stroke recovery. Understanding the epigenetic underpinnings of IS that explicitly alter the brain transcriptomes could open new vistas of therapeutic opportunity. In the current review, we present an update on various aspects linking mitochondrial energy metabolism, oxidative stress and epigenetic modifications in the pathological setting of IS.

中文翻译：

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缺血性脑卒中线粒体代谢与氧化应激之间的相互作用：表观遗传学联系。

表观遗传学的出现带来了构造上的转变，使人们对诸如缺血性中风（IS）等复杂疾病的分子基础有了更深入的了解。对神经退行性疾病的表观遗传基础的大量科学探究支持了这样一种观点，即碳流量改变为中心碳代谢，并且氧化还原状态受到干扰，通过随机表观遗传变化控制了伴随的转录谱。鉴于对IS中线粒体能量代谢，氧化应激和表观遗传学之间的联系的日益了解，迄今未被充分认识的“神经能量学”一直受到关注。IS期间定义的新陈代谢转变必定是Krebs循环和其他途径（例如，乙酰-CoA，柠檬酸盐，2-氧-戊二酸盐，琥珀酸盐，神经元线粒体中的富马酸酯，S-腺苷甲硫氨酸，β-羟基丁酸酯和辅因子（NAD +，FAD，ATP，维生素C）。这些改变通过调节几种染色质修饰酶的活性而影响细胞转录组，这些染色质修饰酶通过DNA甲基化的改变和组蛋白翻译后的修饰而引起表观基因组的转变。这触发了下游信号传导级联反应，在IS过程中引起了适应性反应和细胞死亡反应。实际上，它们在卒中后恢复过程中还具有神经网络功能，大脑可塑性和神经发生方面的优势。了解IS的表观遗传基础可显着改变大脑转录组，这可能会打开治疗机会的新视野。在当前的评论中，我们提出了有关线粒体能量代谢的各个方面的最新动态，