Corrigendum to “Lithium ameliorates spinal cord injury through endoplasmic reticulum stress-regulated autophagy and alleviated apoptosis through IRE1 and PERK/eIF2α signaling pathways” [J Neurorestoratol 11 (2023) 100081]

This article is a corrigendum — a formal published correction — to an earlier 2023 study investigating whether lithium, a long-used mood-stabilizing drug, can help repair damage after spinal cord injury (SCI). The original research proposed that lithium works partly by activating a cellular 'self-cleaning' process called autophagy, while also reducing a harmful stress response in a cell compartment called the endoplasmic reticulum (ER). Two molecular signaling arms — IRE1 and PERK/eIF2α — were identified as key mediators of this protective effect. The corrigendum itself does not change the scientific conclusions but corrects errors in the previously published version, such as mislabeled figures, author details, or data presentation. Because the underlying science remains relevant, the corrected record matters for researchers building on this work. Lithium's dual role in modulating both ER stress and autophagy is of growing interest in neurorestoration, given how few effective SCI treatments exist. The study was conducted in an animal model, which places it at a preliminary-to-emerging evidence tier pending human translation.

• Lithium treatment was reported to reduce ER stress-triggered apoptosis (programmed cell death) in spinal cord injury models by modulating the IRE1 and PERK/eIF2α signaling axes — specific effect sizes are not recoverable from the corrigendum notice alone (best-effort flag: low confidence on exact numbers).
• Autophagy induction was identified as a mechanistic bridge between ER stress and neuroprotection, suggesting lithium co-opts a cellular recycling pathway to limit secondary injury after SCI.
• The corrigendum formally corrects the 2023 publication record without altering core scientific conclusions; the nature of the specific correction (e.g., figure labeling, data tables) is not detailed in the available metadata.

The underlying study used an animal model of spinal cord injury (rodent, species not confirmed from available metadata) with lithium administered as the pharmacological intervention. Molecular endpoints included markers of ER stress (IRE1, PERK, eIF2α phosphorylation), autophagic flux, and apoptosis. This corrigendum record (DOI: 10.1016/j.jnrt.2026.100291) references and corrects the original article published in Journal of Neurorestoratology 11 (2023) 100081; full sample sizes and follow-up durations are drawn from that original report and are not independently restated here. Methods details should be verified against the corrected original article — best-effort assessment given thin corrigendum metadata.

As a corrigendum, this article cannot itself advance new evidence; its scientific limitations are those of the original 2023 animal study, including the absence of human or primate data and uncertainty about whether lithium's therapeutic window in SCI translates to clinical doses tolerable in humans. The reliance on a single animal model limits generalizability, and the mechanistic pathway (IRE1/PERK-driven autophagy) would benefit from genetic knockout validation to confirm causality. The nature and scope of the correction itself are opaque from the corrigendum DOI alone, which limits confidence in knowing whether any quantitative results were affected. Future experiments using conditional IRE1 or PERK knockout animals, or human iPSC-derived spinal neuron models, would substantially clarify mechanism and translational potential.

This corrected study extends the autophagy-in-neurological-injury theme explored by [§128], which similarly examines autophagy modulation (via iTBS) in a neurological context, offering a pharmacological parallel to that neuromodulatory approach. It parallels [§37], where autophagic clearance of protein aggregates is driven by specific molecular mediators (GABARAPs/CHCHD proteins), reinforcing the broader corpus thesis that selective autophagy pathways can be therapeutically targeted in neurodegeneration and injury. The ER-stress-to-autophagy signaling logic here also parallels [§38] (mammalian lysophagy mechanisms), since both studies situate autophagy induction downstream of organelle stress signals. Because the evidence base is an animal model corrigendum with low metadata confidence, corpus placement is preliminary, and direct mechanistic contradictions with other listed articles cannot be established from available information.

• Intermittent Theta-Burst Stimulation (iTBS) Improves Motor Coordination and Modulates Neuroinflammation and Autophagy in SCA3/MJD Mice
  Both target autophagy as a neuroprotective mechanism in CNS injury models — comparing pharmacological (lithium/ER stress) vs. neurostimulation (iTBS) routes to the same endpoint clarifies whether autophagy induction is a shared final pathway.
• CHCHD2 and CHCHD10 promoted autophagic clearance of protein aggregates via GABARAPs
  CHCHD2/CHCHD10-driven autophagic clearance via GABARAPs shares the theme of molecularly-specific autophagy induction for neuroprotection, providing a mechanistic comparator to IRE1/PERK-mediated autophagy in SCI.
• Mammalian Lysophagy: mechanisms and pathophysiological implications
  Mammalian lysophagy mechanisms illuminate how organelle stress (lysosomal damage vs. ER stress here) triggers selective autophagy, making this a useful mechanistic contrast to the PERK/eIF2α axis described in the lithium SCI study.
• FOXO transcription factors in Alzheimer's Disease: balancing neuroprotection and neuronal degeneration
  FOXO transcription factors balance neuroprotection and neurodegeneration partly through autophagy regulation — comparing FOXO-mediated vs. ER-stress-mediated autophagy induction helps situate lithium's mechanism within the broader neuroprotective signaling landscape.