ArticleFrontiers in molecular neuroscience2025
Silencing ATF3 mediates mitochondrial homeostasis and improves ischemic stroke through regulating the MAPK signaling pathway.
Article in Frontiers in molecular neuroscience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- BTG2 knockdown attenuates oxygen-glucose deprivation/reoxygenation-induced injury and apoptosis in PC12 cells: an effect associated with MAPK pathway inhibition.Molecular biology reports · 2026Article
- Intracellular Calcium Overload Promotes NFATc1-ATF3 Activation and Induces the Senescence-Associated Phenotype in Irradiated Osteocytes.Life (Basel, Switzerland) · 2026Article
Corrections and comments
- Erratum issued
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitochondrial homeostasis is crucial for preventing and treatment of ischemic stroke. This study aimed to investigate the role of activating transcription factor 3 (ATF3) in ischemic stroke and mitochondrial homeostasis. ATF3 was silenced in oxygen glucose deprivation/reperfusion (OGD/R)-treated HT22 cells to evaluate its effects on cell apoptosis and mitochondrial function. The effects of silencing ATF3 on neurological injury, infarction, adenosine triphosphate (ATP), nicotinamide adenine dinucleotide (NAD+), mitofusin 1 (MFN1) and MFN2 were evaluated in stroke rats. Transcriptome sequencing and differential expression analysis were conducted to identify differential expressed genes (DEGs) associated with silencing ATF3, followed by functional enrichment analysis. The mitogen activated protein kinase (MAPK) agonist, anisomycin, was used to investigate the regulation of ATF3 in ischemic stroke and mitochondrial homeostasis via the MAPK pathway. Silencing ATF3 increased cell viability and inhibited apoptosis of OGD/R-induced cells. In stroke rats, silencing ATF3 reduced brain water content, decreased neurological injury and alleviated cerebral infarction. Notably, silencing ATF3 significantly inhibited the production of reactive oxygen species (ROS), increased the concentrations of ATP and NAD+, and upregulated the expression of MFN1 and MFN2. Next, 4,517 DGEs associated with silencing ATF3 were mainly enriched in MAPK signaling pathway. Silencing ATF3 downregulated the expression of phosphorylation-extracellular signal-regulated kinase (p-ERK)/ERK in OGD/R cells. Anisomycin notably reversed the effect of silencing ATF3 on ischemic stroke and mitochondrial homeostasis. Silencing ATF3 attenuates ischemic stroke and improves mitochondrial homeostasis via the MAPK signaling pathway, which shares a novel direction for maintaining mitochondrial homeostasis in ischemic stroke.
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