Association Study Between Genetic Variation in Whole Mitochondrial Genome and Ischemic Stroke

Luan, Yingying; Yang, Dongzhi; Zhang, Zhaojing; Bie, Xiaoshuai; Zhao, Hang; Wang, Yuanli; Liu, Yang; Yang, Shangdong; Zhou, Baixue; Xu, Yan; Zheng, Hong; He, Ying

doi:10.1007/s12031-020-01778-3

Cited by 4 publications

(3 citation statements)

References 26 publications

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“…However, mitochondria are very sensitive to ischemia and hypoxia ( 26 ); under these circumstances, they undergo significant alterations, including Ca 2+ influx, mitochondrial permeability transition pore (mPTP) opening, reactive oxygen species (ROS) generation, DNA damage and mutation, unbalanced mitochondrial dynamics, and aberrant mitochondrial position ( 27 - 29 ). These changes in mitochondria are termed as mitochondrial dysfunction, which is strongly implicated in patients and multiple animal models with ischemic stroke ( 30 - 34 ).…”

Section: Pathophysiological Changes Of Mitochondria In Ischemic Strokementioning

confidence: 99%

“…mtDNA is markedly more prone to mutations than nuclear DNA ( 58 ). Particularly, the frequency of mtDNA mutations was found to be significantly higher in the brain of patients with ischemic stroke, and numerous of these mutations resulted in an alteration of amino acid therefore structure of protein ( 34 ). The vulnerability of mtDNA to mutation is due to its lacking of high-fidelity repair processes, the high-copy-number of mtDNA within each cell, and the close proximity to ROS-generating machinery ( 59 ).…”

Section: Pathophysiological Changes Of Mitochondria In Ischemic Strokementioning

confidence: 99%

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Focus on the role of mitochondria in NLRP3 inflammasome activation: A prospective target for the treatment of ischemic stroke (Review)

et al. 2022

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Post-ischemic neuroinflammation induced by the innate local immune response is a major pathophysiological feature of cerebral ischemic stroke, which remains the leading cause of mortality and disability worldwide. NLR family pyrin domain containing (NLRP)3 inflammasome crucially mediates post-ischemic inflammatory responses via its priming, activation and interleukin-1β release during hypoxic-ischemic brain damage. Mitochondrial dysfunctions are among the main hallmarks of several brain diseases, including ischemic stroke. In the present review, focus was addressed on the role of mitochondria in cerebral ischemic stroke while keeping NLRP3 inflammasome as a link. Under ischemia and hypoxia, mitochondria are capable of controlling NLRP3 inflammasome-mediated neuroinflammation through mitochondrial released contents, mitochondrial localization and mitochondrial related proteins. Thus, inflammasome and mitochondria may be attractive targets to treat ischemic stroke as well as the several drugs that target the process of mitochondrial function to treat cerebral ischemic stroke. At present, certain drugs have already been studied in clinical trials.

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Section: Pathophysiological Changes Of Mitochondria In Ischemic Strokementioning

confidence: 99%

Section: Pathophysiological Changes Of Mitochondria In Ischemic Strokementioning

confidence: 99%

Focus on the role of mitochondria in NLRP3 inflammasome activation: A prospective target for the treatment of ischemic stroke (Review)

et al. 2022

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“…Additionally, mutation of gene-encoded subunits in mtDNA results in increased ROS generation, which makes mtDNA more susceptible to mutations than nuclear DNA ( Zhang et al, 2022 ). Researchers have reported that the frequency of mtDNA mutations was significantly higher in the brains of patients with ischemic stroke ( Luan et al, 2021 ). In summary, the ischemic stroke cascade involves changes in mitochondrial function and structure, indicating that mitochondrial structure and function play a critical role in the pathogenesis of ischemic stroke.…”

Section: The Role Of Mitochondria In Ischemic Strokementioning

confidence: 99%

Traditional Chinese medicine in treating ischemic stroke by modulating mitochondria: A comprehensive overview of experimental studies

et al. 2023

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Ischemic stroke has been a prominent focus of scientific investigation owing to its high prevalence, complex pathogenesis, and difficulties in treatment. Mitochondria play an important role in cellular energy homeostasis and are involved in neuronal death following ischemic stroke. Hence, maintaining mitochondrial function is critical for neuronal survival and neurological improvement in ischemic stroke, and mitochondria are key therapeutic targets in cerebral stroke research. With the benefits of high efficacy, low cost, and high safety, traditional Chinese medicine (TCM) has great advantages in preventing and treating ischemic stroke. Accumulating studies have explored the effect of TCM in preventing and treating ischemic stroke from the perspective of regulating mitochondrial structure and function. In this review, we discuss the molecular mechanisms by which mitochondria are involved in ischemic stroke. Furthermore, we summarized the current advances in TCM in preventing and treating ischemic stroke by modulating mitochondria. We aimed to provide a new perspective and enlightenment for TCM in the prevention and treatment of ischemic stroke by modulating mitochondria.

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Cell-free circulating mitochondrial DNA: An emerging biomarker for airborne particulate matter associated with cardiovascular diseases

Rehman

Kumari

Kamthan³

et al. 2023

Free Radical Biology and Medicine

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Association Study Between Genetic Variation in Whole Mitochondrial Genome and Ischemic Stroke

Cited by 4 publications

References 26 publications

Focus on the role of mitochondria in NLRP3 inflammasome activation: A prospective target for the treatment of ischemic stroke (Review)

Focus on the role of mitochondria in NLRP3 inflammasome activation: A prospective target for the treatment of ischemic stroke (Review)

Traditional Chinese medicine in treating ischemic stroke by modulating mitochondria: A comprehensive overview of experimental studies

Cell-free circulating mitochondrial DNA: An emerging biomarker for airborne particulate matter associated with cardiovascular diseases

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