ArticleJournal of advanced research2025
Actl6a regulates autophagy via Sox2-dependent Atg5 and Atg7 expression to inhibit apoptosis in spinal cord injury.
Article in Journal of advanced research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Nanomaterial-driven spatiotemporal autophagy modulation: The dual-edged sword in precision cancer therapy.Acta pharmaceutica Sinica. B · 2026Review
- 6-gingerol Attenuates Inflammatory Response in Rats With Spinal Cord Injury by Reducing NLRP3-mediated Microglial Pyroptosis.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2026Article
- Role of Autophagy in Goose Astrovirus-Induced Renal Injury in Goslings.Animals : an open access journal from MDPI · 2026Article
- PTGS2 as a potential target for apigenin to promote spinal cord injury repair.Journal of bioenergetics and biomembranes · 2026Article
- Mesenchymal Stem Cell-Derived Exosomes: A Promising Therapeutic Strategy for Spinal Cord Injury.International journal of nanomedicine · 2025Review
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Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionSpinal cord injury (SCI) is a severe central nervous system disorder with limited treatment options. While autophagy plays a protective role in neural repair, its regulatory mechanisms in SCI remain unclear. Actin-like protein 6A (Actl6a) influences cell fate and neural development, yet its specific role in SCI repair is not well understood. This study investigates Actl6a's function in regulating autophagy and apoptosis via the transcription factor Sox2 in SCI.
objectivesThis study aims to determine if Actl6a promotes neural survival post-SCI by regulating autophagy-related genes Atg5 and Atg7 through Sox2. It also examines how the demethylase Fto modulates Actl6a mRNA stability via m6A methylation.
methodsIn vitro experiments were conducted using primary neurons and HT-22 hippocampal cells exposed to hydrogen peroxide (H
resultsActl6a expression significantly decreased after SCI, resulting in increased apoptosis. Overexpressing Actl6a enhanced autophagy, reduced apoptosis, and improved neurological function in SCI models. Mechanistically, Actl6a and Sox2 collaboratively upregulated Atg5 and Atg7 expression, promoting autophagy. Fto's modulation of Actl6a mRNA stability via m6A demethylation further influenced autophagy and apoptosis.
conclusionActl6a, through interaction with Sox2, plays a critical role in modulating autophagy and reducing apoptosis in SCI, with Fto's m6A modification affecting Actl6a stability. This Fto/Actl6a/Sox2 axis is a promising therapeutic target for SCI repair.
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