RT Journal Article
SR Electronic
T1 Dual regulation of Atf3 and Lonp1 as therapeutic targets in cerebral ischaemia-reperfusion injury
JF Stroke and Vascular Neurology
JO Stroke Vasc Neurol
FD BMJ Publishing Group Ltd
SP svn-2024-003324
DO 10.1136/svn-2024-003324
A1 Fan, Weijian
A1 Zhou, Min
A1 Zhou, Lin
A1 Tong, Jindong
A1 Tan, Jinyun
A1 Shi, Weihao
A1 Yu, Bo
YR 2025
UL http://svn.bmj.com/content/early/2025/03/05/svn-2024-003324.abstract
AB Background Cerebral ischemia-reperfusion injury (CIRI) leads to cognitive dysfunction, neuronal death, and inflammation. Understanding the molecular mechanisms underlying CIRI is crucial for developing effective therapeutic strategies.Objective This study aims to investigate the roles of activating transcription factor 3 (Atf3) and lon protease homolog 1 (Lonp1) in CIRI, particularly focusing on how Atf3 regulates Lonp1 expression and its effects on mitochondrial function.Methods Single-cell transcriptomics and proteomic analyses were employed to explore Atf3's influence on Lonp1 and its subsequent impact on neuronal survival and apoptosis.Results The findings indicate that Atf3 plays a crucial role in modulating Lonp1 expression, which in turn affects mitochondrial function, neuronal survival, and apoptotic pathways.Conclusion This study provides new insights into the regulatory mechanisms of Atf3 and Lonp1 in CIRI, identifying potential therapeutic targets for managing ischemic brain injury and neurodegenerative diseases.Data are available upon reasonable request. The data underlying this article will be shared on reasonable request to the corresponding author.