<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Yue WWS</submitter><funding>NINDS NIH HHS</funding><pagination>407-414</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC12935313</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>634(8033)</volume><pubmed_abstract>After injury, mammalian spinal cords develop scars to confine the lesion and prevent further damage. However, excessive scarring can hinder neural regeneration and functional recovery&lt;sup>1,2&lt;/sup>. These competing actions underscore the importance of developing therapeutic strategies to dynamically modulate scar progression. Previous research on scarring has primarily focused on astrocytes, but recent evidence has suggested that ependymal cells also participate. Ependymal cells normally form the epithelial layer encasing the central canal, but they undergo massive proliferation and differentiation into astroglia following certain injuries, becoming a core scar component&lt;sup>3-7&lt;/sup>. However, the mechanisms regulating ependymal proliferation in vivo remain unclear. Here we uncover an end</pubmed_abstract><journal>Nature</journal><pubmed_title>Endogenous opioid signalling regulates spinal ependymal cell proliferation.</pubmed_title><pmcid>PMC12935313</pmcid><funding_grant_id>R35 NS105038</funding_grant_id><pubmed_authors>Touhara KK</pubmed_authors><pubmed_authors>Julius D</pubmed_authors><pubmed_authors>Yue WWS</pubmed_authors><pubmed_authors>Toma K</pubmed_authors><pubmed_authors>Duan X</pubmed_authors></additional><is_claimable>false</is_claimable><name>Endogenous opioid signalling regulates spinal ependymal cell proliferation.</name><description>After injury, mammalian spinal cords develop scars to confine the lesion and prevent further damage. However, excessive scarring can hinder neural regeneration and functional recovery&lt;sup>1,2&lt;/sup>. These competing actions underscore the importance of developing therapeutic strategies to dynamically modulate scar progression. Previous research on scarring has primarily focused on astrocytes, but recent evidence has suggested that ependymal cells also participate. Ependymal cells normally form the epithelial layer encasing the central canal, but they undergo massive proliferation and differentiation into astroglia following certain injuries, becoming a core scar component&lt;sup>3-7&lt;/sup>. However, the mechanisms regulating ependymal proliferation in vivo remain unclear. Here we uncover an end</description><dates><release>2024-01-01T00:00:00Z</release><publication>2024 Oct</publication><modification>2026-07-16T20:47:10.315Z</modification><creation>2026-07-10T03:12:25.542Z</creation></dates><accession>S-EPMC12935313</accession><cross_references><pubmed>39294372</pubmed><doi>10.1038/s41586-024-07889-w</doi></cross_references></HashMap>