Mitochondrial dysfunction arises from an inadequate number of mitochondria, an inability to provide necessary substrates to mitochondria, or a dysfunction in their electron transport and a denosine triphosphate synthesis machinery. Occurrences of mitochondrial dysfunction are due to genetic or environmental changes in the mitochondria or in the nuclear DNA that codes mitochondrial components. Currently, drug options are available, yet no treatment exists in sight of this disease and needs a new insight into molecular and signaling pathways for this disease. microRNAs (miRNAs) are small, endogenous, and noncoding RNAs function as a master regulator of gene expression. The evolution of miRNAs in the past two decades emerged as a key regulator of gene expression that controls physiological pathological cellular differentiation processes, and metabolic homeostasis such as development and cancer. It has been known that miRNAs are a potential biomarker in both communicable and noncommunicable diseases. But, in the case of mitochondrial dysfunction in miRNAs, the number of studies and investigations are comparatively less than those on other diseases and dysfunctions. In this review, we have elaborated the roles of miRNAs in the mitochondrial diseases and dysfunctions.

中文翻译：

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microRNA在线粒体疾病/功能障碍中的生物学和临床意义。

线粒体功能异常是由于线粒体数量不足，无法为线粒体提供必需的底物或电子传输功能异常以及三磷酸腺苷合成机制所致。线粒体功能障碍的发生是由于线粒体或编码线粒体成分的核DNA的遗传或环境变化。当前，有药物可供选择，但尚无针对该疾病的治疗方法，并且需要对该疾病的分子和信号传导途径有新的认识。microRNA（miRNA）小，内源，非编码RNA充当基因表达的主要调控因子。在过去的二十年里，miRNA的进化成为控制生理病理细胞分化过程的基因表达的关键调节因子，和代谢稳态，例如发育和癌症。已知miRNA在传染病和非传染病中都是潜在的生物标志物。但是，就miRNA中的线粒体功能障碍而言，与其他疾病和功能障碍相比，研究和调查的数量相对较少。在这篇综述中，我们详细阐述了miRNA在线粒体疾病和功能障碍中的作用。