<HashMap><database>bioimages</database><scores/><additional><omics_type>Unknown</omics_type><submitter/><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-BIAD652</full_dataset_link><repository>bioimages</repository><figure_sub>Specimen</figure_sub><figure_sub>Study Component</figure_sub><figure_sub>organisation</figure_sub><figure_sub>Biosample</figure_sub><figure_sub>Associations</figure_sub><figure_sub>Image acquisition</figure_sub><pubmed_authors>Felipe Court</pubmed_authors></additional><is_claimable>false</is_claimable><name>Senescent Schwann cells induced by aging and chronic denervation impair axonal regeneration after peripheral nerve injury</name><description>After peripheral nerve injuries, successful axonal growth and functional recovery requires the reprogramming of Schwann cells into a reparative phenotype, a process dependent on the activation of the transcription factor c-Jun. Nevertheless, axonal regeneration is greatly impaired in aged organisms or after chronic denervation leading to important clinical problems. This regenerative failure has been associated to a diminished c-Jun expression by Schwann cells, but whether the inability of these cells to maintain a repair state is associated to the transition into a phenotype inhibitory for axonal growth, has not been evaluated so far. We find that repair Schwann cells transitions into a senescent phenotype, characterized by diminished c-Jun expression and secretion of factor inhibitory fo</description><dates><release>2023-03-17T00:00:00Z</release><modification>2023-03-21T10:50:54.926Z</modification><creation>2023-03-21T10:50:54.926Z</creation></dates><accession>S-BIAD652</accession><cross_references/></HashMap>