Mitochondria and Eye

L. Singh, Mithalesh Kumar Singh
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引用次数: 2

Abstract

Mitochondria are essential subcellular organelles and important key regulators of metabolism. Mammalian mitochondria contain their own DNA (mtDNA). Human mtDNA is remarkably small (16,569 bp) compared to nuclear DNA. Mitochondria promote aerobic respiration, an important part of energy metabolism in eukaryotes, as the site of oxidative phosphorylation (OXPHOS). OXPHOS occurs in the inner membrane of the mitochondrion and involves 5 protein complexes that sequentially undergo reduction-oxygen reactions ultimately producing adenosine triphosphate (ATP). Tissues with high metabolic demand such as lungs, central nervous system, peripheral nerves, heart, adrenal glands, renal tubules and the retina are affected preferentially by this critical role in energy production by mitochondrial disorders. Eye-affected mitochondrial disorders are always primary, but the role of mitochondrial dysfunction is now best understood in acquired chronic progressive ocular diseases. Recent advances in mitochondrial research have improved our understanding of ocular disorders. In this chapter, we will discuss the mitochondria in relation to eye diseases, ocular tumors, pathogenesis, and treatment modalities that will help to improve the outcomes of these conditions.
线粒体与眼睛
线粒体是重要的亚细胞细胞器和重要的代谢关键调节剂。哺乳动物线粒体含有自己的DNA (mtDNA)。与核DNA相比,人类mtDNA非常小(16,569 bp)。线粒体作为氧化磷酸化(OXPHOS)的位点,促进有氧呼吸,是真核生物能量代谢的重要组成部分。OXPHOS发生在线粒体的内膜中,涉及5种蛋白质复合物,它们依次进行还原-氧反应,最终产生三磷酸腺苷(ATP)。具有高代谢需求的组织,如肺、中枢神经系统、周围神经、心脏、肾上腺、肾小管和视网膜,优先受到线粒体疾病在能量产生中的关键作用的影响。影响眼睛的线粒体疾病总是主要的,但线粒体功能障碍的作用现在被最好地理解为获得性慢性进行性眼病。线粒体研究的最新进展提高了我们对眼部疾病的理解。在本章中,我们将讨论线粒体与眼病、眼肿瘤、发病机制和治疗方式的关系,这将有助于改善这些疾病的结果。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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