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REVIEW article

Front. Immunol.
Sec. Inflammation
Volume 15 - 2024 | doi: 10.3389/fimmu.2024.1460286
This article is part of the Research Topic Exploring Cardiovascular and Cerebrovascular Diseases Interaction with Inflammation: Biomarkers, Drug Targets, and Personalized Treatments through Multi-omics Data Integration View all 4 articles

Mitophagy-associated programmed neuronal death and neuroinflammation

Provisionally accepted
Yanlin Zhu Yanlin Zhu Jianning Zhang Jianning Zhang Quanjun Deng Quanjun Deng Xin Chen Xin Chen *
  • Tianjin Medical University General Hospital, Tianjin, China

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

    Mitochondria are crucial organelles that play a central role in cellular metabolism and programmed cell death in eukaryotic cells. Mitochondrial autophagy (mitophagy) is a selective process where damaged mitochondria are encapsulated and degraded through autophagic mechanisms, ensuring the maintenance of both mitochondrial and cellular homeostasis. Excessive programmed cell death in neurons can result in functional impairments following cerebral ischemia and trauma, as well as in chronic neurodegenerative diseases, leading to irreversible declines in motor and cognitive functions. Neuroinflammation, an inflammatory response of the central nervous system to factors disrupting homeostasis, is a common feature across various neurological events, including ischemic, infectious, traumatic, and neurodegenerative conditions.Emerging research suggests that regulating autophagy may offer a promising therapeutic avenue for treating certain neurological diseases. Furthermore, existing literature indicates that various small molecule autophagy regulators have been tested in animal models and are linked to neurological disease outcomes. This review explores the role of mitophagy in programmed neuronal death and its connection to neuroinflammation.

    Keywords: mitophagy, Apoptosis, necroptosis, pyroptosis, ferroptosis, Neuroinflammation

    Received: 05 Jul 2024; Accepted: 10 Sep 2024.

    Copyright: © 2024 Zhu, Zhang, Deng and Chen. 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: Xin Chen, Tianjin Medical University General Hospital, Tianjin, 300052, 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.