<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Pan D</submitter><funding>U.S. Department of Health &amp; Human Services | NIH | National Institute on Aging (U.S. National Institute on Aging)</funding><pagination>27</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC12936232</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>14(1)</volume><pubmed_abstract>Spinal cord injury (SCI) often causes long-term disability. But effective means to promote proper regeneration after SCI has so far failed to reach the clinic. Here, we report that fibrotic scar formation at injury sites prevents recovery after SCI and that the inhibition of fibrotic scar formation significantly improved SCI recovery in adult mice. We found that after SCI there is an elevation of macrophages, which are a primary source of activated transforming growth factor-β 1 (TGF-β1) that in turn recruits mesenchymal stromal/stem cells (MSCs) to induce their fibroblast differentiation, thus promoting scar formation. We also found that activated TGF-β1 acts on resident pericytes in the endothelial niche of the blood-spinal cord barrier to promote their differentiation into fibroblasts, </pubmed_abstract><journal>Bone research</journal><pubmed_title>TGF-β-induced fibrotic scar formation limits recovery of spinal cord injury.</pubmed_title><pmcid>PMC12936232</pmcid><funding_grant_id>R01AG076783</funding_grant_id><funding_grant_id>P01AG066603</funding_grant_id><funding_grant_id>R01AG068997</funding_grant_id><pubmed_authors>Pan D</pubmed_authors><pubmed_authors>Cao X</pubmed_authors><pubmed_authors>Noller K</pubmed_authors><pubmed_authors>Wu P</pubmed_authors><pubmed_authors>Cahan P</pubmed_authors></additional><is_claimable>false</is_claimable><name>TGF-β-induced fibrotic scar formation limits recovery of spinal cord injury.</name><description>Spinal cord injury (SCI) often causes long-term disability. But effective means to promote proper regeneration after SCI has so far failed to reach the clinic. Here, we report that fibrotic scar formation at injury sites prevents recovery after SCI and that the inhibition of fibrotic scar formation significantly improved SCI recovery in adult mice. We found that after SCI there is an elevation of macrophages, which are a primary source of activated transforming growth factor-β 1 (TGF-β1) that in turn recruits mesenchymal stromal/stem cells (MSCs) to induce their fibroblast differentiation, thus promoting scar formation. We also found that activated TGF-β1 acts on resident pericytes in the endothelial niche of the blood-spinal cord barrier to promote their differentiation into fibroblasts, </description><dates><release>2026-01-01T00:00:00Z</release><publication>2026 Feb</publication><modification>2026-07-16T22:09:10.024Z</modification><creation>2026-07-11T03:11:47.052Z</creation></dates><accession>S-EPMC12936232</accession><cross_references><pubmed>41741406</pubmed><doi>10.1038/s41413-026-00507-7</doi></cross_references></HashMap>