ArticleExperimental neurology2025
Morphological regulation of wound repair astrocytes by leucine zipper-bearing kinase-AKT signaling after spinal cord injury.
Article in Experimental neurology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed.
- Astrocyte-microglia crosstalk via CSF1 and IFN-β promotes central nervous system repair.Cell reports · 2026Article
- DLK inhibition has sex-specific effects on neuroprotection and locomotor recovery after spinal cord injury.Experimental neurology · 2026Article
- Targeting the glial-fibrotic scar microenvironment after spinal cord injury: From integrated protection to systematic regulation of regenerative balance.Journal of orthopaedic translation · 2026Review
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
Following focal CNS injury, a salient feature of astrocytes lining the lesion is their remarkable morphological transformation into an interwoven cellular border that serves their protective function in wound closure. Despite the importance of morphology in determining function of lesion border astrocytes and injury outcome, there is sparse knowledge of how cell shape is regulated temporally and mechanistically in border-forming astrocytes. We report a transcriptional program of actin and microtubule reorganization that is induced in lesion border astrocytes after spinal cord injury in mice. By genetic gain- and loss-of-function analyses in vivo, we show that leucine zipper-bearing kinase (LZK) is a positive regulator of injury-responsive transcription of cytoskeleton remodeling genes in lesion border astrocytes, with consequences on morphological adaptation of border-forming astrocytes. Functional validation of LZK-dependent cytoskeleton rearrangement in vitro demonstrates its ability to enhance astrocytic process extension, cell movement, and associated structural reorganization of actin and microtubules. We further identify LZK-dependent activation of AKT in astrocytes invitro and in vivo, which is required for transcriptional regulation of the cytoskeleton by LZK, and to a similar extent as STAT3. Lastly, loss of astrocytic LZK impairs motor recovery after spinal cord injury. Our findings define temporal and molecular regulation of morphological transformation of lesion border astrocytes that may be targeted for CNS repair.
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