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REVIEW article

Front. Mol. Neurosci.
Sec. Brain Disease Mechanisms
Volume 17 - 2024 | doi: 10.3389/fnmol.2024.1394932
This article is part of the Research Topic Oxytosis/Ferroptosis: Unraveling the Mechanisms and Its Multifaceted Role in Neurodegenerative Diseases View all articles

Mechanisms of mitophagy and oxidative stress in cerebral ischemiareperfusion, vascular dementia, and Alzheimer's disease

Provisionally accepted
LV Yu Jie LV Yu Jie 1MENG Zhipeng MENG Zhipeng 1*HU Yunyun HU Yunyun 1*JIANG Bing JIANG Bing 1*YANG Jiao YANG Jiao 1*CHEN Yiqin CHEN Yiqin 1*ZHOU Jun ZHOU Jun 2*LI Mingcheng LI Mingcheng 3*WANG Huping WANG Huping 1,4,5*
  • 1 Gansu University of Chinese Medicine, Lanzhou, China
  • 2 Xichang Hospital of Traditional Chinese Medicine, Xichang, China
  • 3 Qujing Sixty-nine Hospital, Qujing, China
  • 4 Gansu Province Key Laboratory of Traditional Chinese Medicine Mining and Innovation, Lanzhou, China
  • 5 Gansu Provincial Laboratory of New Traditional Chinese Medicine Product Creation Engineering, Lanzhou, China

The final, formatted version of the article will be published soon.

    Neurological diseases have consistently represented a significant challenge in both clinical treatment and scientific research. As research has progressed, the significance of mitochondria in the pathogenesis and progression of neurological diseases has become increasingly prominent.Mitochondria serve not only as a source of energy, but also as regulators of cellular growth and death.Both oxidative stress and mitophagy are intimately associated with mitochondria, and there is mounting evidence that mitophagy and oxidative stress exert a pivotal regulatory influence on the pathogenesis of neurological diseases.In recent years, there has been a notable rise in the prevalence of cerebral ischemia/reperfusion injury (CI/RI), vascular dementia (VaD), and Alzheimer's disease (AD), which collectively represent a significant public health concern.Reduced levels of mitophagy have been observed in CI/RI, VaD and AD. The improvement of associated pathology has been demonstrated through the increase of mitophagy levels. CI/RI results in cerebral tissue ischemia and hypoxia, which causes oxidative stress, disruption of the blood-brain barrier (BBB) and damage to the cerebral vasculature. The BBB disruption and cerebral vascular injury may induce or exacerbate VaD to some extent. In addition, inadequate cerebral perfusion due to vascular injury or altered function may exacerbate the accumulation of amyloid β (Aβ) thereby contributing to or exacerbating AD pathology. Intravenous tissue plasminogen activator (tPA; alteplase) and endovascular thrombectomy are effective treatments for stroke. However, there is a narrow window of opportunity for the administration of tPA and thrombectomy, which results in a markedly elevated incidence of disability among patients with CI/RI. It is regrettable that there are currently no there are still no specific drugs for VaD and AD. Despite the availability of the U.S. Food and Drug Administration(FDA)-approved clinical first-line drugs for AD, including memantine, donepezil hydrochloride, and galantamine, these agents do not fundamentally block the pathological process of AD.In this paper, we undertake a review of the mechanisms of mitophagy and oxidative stress in neurological disorders, a summary of the clinical trials conducted in recent years, and a proposal for a new strategy for targeted treatment of neurological disorders based on both mitophagy and oxidative stress.

    Keywords: mitophagy, Oxidative Stress, Cerebral ischemia/reperfusion, Vascular Dementia, Alzheimer's disease

    Received: 02 Mar 2024; Accepted: 23 Jul 2024.

    Copyright: © 2024 Yu Jie, Zhipeng, Yunyun, Bing, Jiao, Yiqin, Jun, Mingcheng and Huping. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

    * Correspondence:
    MENG Zhipeng, Gansu University of Chinese Medicine, Lanzhou, China
    HU Yunyun, Gansu University of Chinese Medicine, Lanzhou, China
    JIANG Bing, Gansu University of Chinese Medicine, Lanzhou, China
    YANG Jiao, Gansu University of Chinese Medicine, Lanzhou, China
    CHEN Yiqin, Gansu University of Chinese Medicine, Lanzhou, China
    ZHOU Jun, Xichang Hospital of Traditional Chinese Medicine, Xichang, China
    LI Mingcheng, Qujing Sixty-nine Hospital, Qujing, China
    WANG Huping, Gansu University of Chinese Medicine, Lanzhou, China

    Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.