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MINI REVIEW article

Front. Pharmacol.
Sec. Neuropharmacology
Volume 15 - 2024 | doi: 10.3389/fphar.2024.1491563
This article is part of the Research Topic Targeting Mitochondrial Dysfunction for the Discovery and Development of Novel CNS Therapies in Rare and Neurodegenerative Diseases View all 4 articles

Autophagy is a promising process for linking inflammation and redox homeostasis in Down syndrome

Provisionally accepted
Xuehai Ma Xuehai Ma 1Weimin Li Weimin Li 2Jun Ma Jun Ma 3Zhongcheng Han Zhongcheng Han 4Shoulong Deng Shoulong Deng 5Sutian Wang Sutian Wang 6*
  • 1 College of Psychology, Xinjiang Normal University, Urumqi, China
  • 2 School of Physical Education and Health, East China Normal University, Shanghai, Shanghai Municipality, China
  • 3 Xinjiang Urumqi Youai hospital, Urumqi, China
  • 4 People's Hospital of Xinjiang Uygur Autonomous Region, Ürümqi, Xinjiang Uyghur Region, China
  • 5 Chinese Academy of Medical Sciences and Peking Union Medical College, Dongcheng, Beijing Municipality, China
  • 6 Institute of Animal Science, Guangdong Academy of Agricultural Sciences, Guangzhou, China

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

    Trisomy 21, characterized by the presence of an additional chromosome 21, leads to a set of clinical features commonly referred to as Down syndrome (DS). The pathological phenotypes observed in DS are caused by a combination of factors, such as mitochondrial dysfunction, neuroinflammation, oxidative stress, disrupted metabolic patterns, and changes in protein homeostasis and signal transduction, and these factors collectively induce neurological alterations. In DS, the triplication of chromosome 21 and the micronuclei arising from the missegregation of chromosomes are closely associated with inflammation and the development of redox imbalance.Autophagy, an essential biological process that affects cellular homeostasis, is a powerful tool to facilitate the degradation of redundant or dysfunctional cytoplasmic components, thereby enabling the recycling of their constituents. Targeting the autophagy process has been suggested as a promising method to balance intracellular inflammation and oxidative stress and improve mitochondrial dysfunction. In this review, we summarize the role of autophagy in regulating inflammation and redox homeostasis in DS and discuss their crosslinks. A comprehensive elucidation of the roles of autophagy in DS offers novel insights for the development of therapeutic strategies aimed at aneuploidy-associated diseases.

    Keywords: Down Syndrome, Autophagy, Inflammation, redox homeostasis, stress signalling

    Received: 05 Sep 2024; Accepted: 23 Sep 2024.

    Copyright: © 2024 Ma, Li, Ma, Han, Deng and Wang. 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: Sutian Wang, Institute of Animal Science, Guangdong Academy of Agricultural Sciences, Guangzhou, 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.