Wellcome Centre for Mitochondrial Research, Translational and Clinical Research Institute, Faculty of Medical Sciences, Newcastle University, Newcastle upon Tyne, UK.
NHS Highly Specialised Services for Rare Mitochondrial Disorders, Royal Victoria Infirmary, Newcastle upon Tyne Hospitals NHS Foundation Trust, Newcastle upon Tyne, UK.
J Pathol. 2021 Jul;254(4):430-442. doi: 10.1002/path.5641. Epub 2021 Mar 26.
Mitochondria play essential roles in numerous metabolic pathways including the synthesis of adenosine triphosphate through oxidative phosphorylation. Clinically, mitochondrial diseases occur when there is mitochondrial dysfunction - manifesting at any age and affecting any organ system; tissues with high energy requirements, such as muscle and the brain, are often affected. The clinical heterogeneity is parallel to the degree of genetic heterogeneity associated with mitochondrial dysfunction. Around 10% of human genes are predicted to have a mitochondrial function, and defects in over 300 genes are reported to cause mitochondrial disease. Some involve the mitochondrial genome (mtDNA), but the vast majority occur within the nuclear genome. Except for a few specific genetic defects, there remains no cure for mitochondrial diseases, which means that a genetic diagnosis is imperative for genetic counselling and the provision of reproductive options for at-risk families. Next-generation sequencing strategies, particularly exome and whole-genome sequencing, have revolutionised mitochondrial diagnostics such that the traditional muscle biopsy has largely been replaced with a minimally-invasive blood sample for an unbiased approach to genetic diagnosis. Where these genomic approaches have not identified a causative defect, or where there is insufficient support for pathogenicity, additional functional investigations are required. The application of supplementary 'omics' technologies, including transcriptomics, proteomics, and metabolomics, has the potential to greatly improve diagnostic strategies. This review aims to demonstrate that whilst a molecular diagnosis can be achieved for many cases through next-generation sequencing of blood DNA, the use of patient tissues and an integrated, multidisciplinary multi-omics approach is pivotal for the diagnosis of more challenging cases. Moreover, the analysis of clinically relevant tissues from affected individuals remains crucial for understanding the molecular mechanisms underlying mitochondrial pathology. © 2021 The Authors. The Journal of Pathology published by John Wiley & Sons, Ltd. on behalf of The Pathological Society of Great Britain and Ireland.
线粒体在许多代谢途径中发挥着重要作用,包括通过氧化磷酸化合成三磷酸腺苷。临床上,当线粒体功能障碍时会发生线粒体疾病 - 表现在任何年龄,并影响任何器官系统;能量需求高的组织,如肌肉和大脑,通常会受到影响。临床异质性与与线粒体功能障碍相关的遗传异质性程度平行。大约 10%的人类基因被预测具有线粒体功能,据报道 300 多个基因的缺陷会导致线粒体疾病。有些涉及线粒体基因组(mtDNA),但绝大多数发生在核基因组内。除了少数特定的遗传缺陷外,线粒体疾病仍然没有治愈方法,这意味着遗传诊断对于遗传咨询和为高危家庭提供生殖选择至关重要。下一代测序策略,特别是外显子组和全基因组测序,彻底改变了线粒体诊断,使得传统的肌肉活检在很大程度上被一种非侵入性的血液样本所取代,这种方法对遗传诊断具有公平性。在这些基因组方法未确定致病缺陷的情况下,或者致病性的证据不足时,需要进行额外的功能研究。补充 'omics' 技术(包括转录组学、蛋白质组学和代谢组学)的应用有可能极大地改善诊断策略。这篇综述旨在表明,虽然通过血液 DNA 的下一代测序可以对许多病例进行分子诊断,但使用患者组织和综合的、多学科的多组学方法对于更具挑战性的病例的诊断至关重要。此外,分析受影响个体的临床相关组织仍然是了解线粒体病理学分子机制的关键。