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dc.contributor.authorGomez-Sanchez, Jose Antonio
dc.contributor.authorPatel, Nikiben
dc.contributor.authorMartirena, Fernanda
dc.contributor.authorFazal, Shaline
dc.contributor.authorMutschler, Clara
dc.contributor.authorCabedo, Hugo
dc.date.accessioned2022-04-25T01:02:35Z
dc.date.available2022-04-25T01:02:35Z
dc.date.issued2022-03-10
dc.identifier.issn1422-0067
dc.identifier.other35328416
dc.identifier.otherPMC8951080
dc.identifier.urihttps://www.repository.cam.ac.uk/handle/1810/336400
dc.description.abstractThe peripheral nervous system (PNS) has a remarkable regenerative capacity in comparison to the central nervous system (CNS), a phenomenon that is impaired during ageing. The ability of PNS axons to regenerate after injury is due to Schwann cells (SC) being reprogrammed into a repair phenotype called Repair Schwann cells. These repair SCs are crucial for supporting axonal growth after injury, myelin degradation in a process known as myelinophagy, neurotropic factor secretion, and axonal growth guidance through the formation of Büngner bands. After regeneration, repair SCs can remyelinate newly regenerated axons and support nonmyelinated ax-ons. Increasing evidence points to an epigenetic component in the regulation of repair SC gene ex-pression changes, which is necessary for SC reprogramming and regeneration. One of these epigenetic regulations is histone acetylation by histone acetyl transferases (HATs) or histone deacetylation by histone deacetylases (HDACs). In this review, we have focused particularly on three HDAC classes (I, II, and IV) that are Zn2+-dependent deacetylases. These HDACs are important in repair SC biology and remyelination after PNS injury. Another key aspect explored in this review is HDAC genetic compensation in SCs and novel HDAC inhibitors that are being studied to improve nerve regeneration.
dc.description.sponsorshipMinisterio de Economía y Competitividad (BFU2016-75864R and PID2019-109762RB-I00) ISABIAL (UGP18-257 and UGP-2019-128) Conselleria Educació Generalitat Valenciana (PROMETEO 2018/114) Medical Research Council (UK) studentship (2251399)
dc.languageeng
dc.publisherMDPI AG
dc.rightsAttribution 4.0 International
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/
dc.sourcenlmid: 101092791
dc.sourceessn: 1422-0067
dc.subjectNerve regeneration
dc.subjectAgeing
dc.subjectSchwann cell
dc.subjectNerve injury
dc.subjectMyelin
dc.subjectRemyelination
dc.subjectHdacs
dc.subjectRepair Schwann Cell
dc.subjectHdacs Therapies
dc.subjectSchwann Cells
dc.subjectAxons
dc.subjectPeripheral Nervous System
dc.subjectHistone Deacetylases
dc.subjectHistones
dc.subjectNerve Regeneration
dc.titleEmerging Role of HDACs in Regeneration and Ageing in the Peripheral Nervous System: Repair Schwann Cells as Pivotal Targets
dc.typeArticle
dc.date.updated2022-04-25T01:02:34Z
prism.issueIdentifier6
prism.publicationNameInternational Journal of Molecular Sciences
prism.volume23
dc.identifier.doi10.17863/CAM.83817
dcterms.dateAccepted2022-03-09
rioxxterms.versionofrecord10.3390/ijms23062996
rioxxterms.versionVoR
rioxxterms.licenseref.urihttps://creativecommons.org/licenses/by/4.0/
dc.contributor.orcidFazal, Shaline [0000-0002-2813-4022]
dc.identifier.eissn1422-0067
pubs.funder-project-idMedical Research Council (2251399)


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Attribution 4.0 International
Except where otherwise noted, this item's licence is described as Attribution 4.0 International