Autism is a heterogeneous neurodevelopmental and neuropsychiatric disorder with no precise etiology. Deficits in cognitive functions uncover at early stages and are known to have an environmental and genetic basis. Since autism is multifaceted and also linked with other comorbidities associated with various organs, there is a possibility that there may be a fundamental cellular process responsible for this. These reasons place mitochondria at the point of interest as it is involved in multiple cellular processes predominantly involving metabolism. Mitochondria encoded genes were taken into consideration lately because it is inherited maternally, has its own genome and also functions the time of embryo development. Various researches have linked mitochondrial mishaps like oxidative stress, ROS production and mt-DNA copy number variations to autism. Despite dramatic advances in autism research worldwide, the studies focusing on mitochondrial dysfunction in autism is rather minimal, especially in India. India, owing to its rich diversity, may be able to contribute significantly to autism research. It is vital to urge more studies in this domain as it may help to completely understand the basics of the condition apart from a genetic standpoint. This review focuses on the worldwide and Indian scenario of autism research; mitochondrial abnormalities in autism and possible therapeutic approaches to combat it.

自闭症是一种异质性的神经发育和神经精神障碍，没有确切的病因。认知功能的缺陷在早期阶段就会发现，并且已知具有环境和遗传基础。由于自闭症是多方面的，并且还与与各种器官相关的其他合并症有关，因此有可能是一个基本的细胞过程导致了这一点。这些原因将线粒体置于关注点，因为它涉及主要涉及新陈代谢的多个细胞过程。线粒体编码基因最近被考虑在内，因为它是母系遗传的，有自己的基因组，并且在胚胎发育时间也起作用。各种研究已将氧化应激、ROS 产生和 mt-DNA 拷贝数变异等线粒体事故与自闭症联系起来。尽管全球自闭症研究取得了巨大进展，但专注于自闭症线粒体功能障碍的研究相当少，尤其是在印度。印度由于其丰富的多样性，可能能够为自闭症研究做出重大贡献。敦促在该领域进行更多研究至关重要，因为它可能有助于从遗传角度完全了解该病症的基础知识。本综述侧重于自闭症研究的全球和印度情景；自闭症中的线粒体异常和可能的治疗方法来对抗它。敦促在该领域进行更多研究至关重要，因为它可能有助于从遗传角度完全了解该病症的基础知识。本综述侧重于自闭症研究的全球和印度情景；自闭症中的线粒体异常和可能的治疗方法来对抗它。敦促在该领域进行更多研究至关重要，因为它可能有助于从遗传角度完全了解该病症的基础知识。本综述侧重于自闭症研究的全球和印度情景；自闭症中的线粒体异常和可能的治疗方法来对抗它。