<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>8(16)</volume><submitter>Huang Y</submitter><pubmed_abstract>Autophagy is a promising target for promoting neural regeneration, which is essential for sensorimotor recovery following traumatic brain injury (TBI). Whether neuronal heat shock protein B2 (HSPB2), a small molecular heat shock protein, reduces injury and promotes recovery following TBI remains unclear. In this study, we demonstrated that HSPB2 was significantly increased in the neurons of a TBI mouse model, patients, and primary neuron cultures subjected to oxygen/glucose deprivation and reperfusion treatment. Upon creating a tamoxifen-induced neuron-specific HSPB2 overexpression transgenic mouse model, we found that elevated HSPB2 levels promoted long-term sensorimotor recovery and alleviated tissue loss after TBI. We also demonstrated that HSPB2 enhanced white matter structural and fun</pubmed_abstract><journal>JCI insight</journal><pagination>e168919</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC10543718</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>HSPB2 facilitates neural regeneration through autophagy for sensorimotor recovery after traumatic brain injury.</pubmed_title><pmcid>PMC10543718</pmcid><pubmed_authors>Meng S</pubmed_authors><pubmed_authors>Li J</pubmed_authors><pubmed_authors>Lyu Y</pubmed_authors><pubmed_authors>Xiang J</pubmed_authors><pubmed_authors>Wu B</pubmed_authors><pubmed_authors>Shi Z</pubmed_authors><pubmed_authors>Wu G</pubmed_authors><pubmed_authors>Xu ZX</pubmed_authors><pubmed_authors>Huang Y</pubmed_authors><pubmed_authors>Hu J</pubmed_authors><pubmed_authors>Gao Y</pubmed_authors><pubmed_authors>Jia X</pubmed_authors><pubmed_authors>Wang Y</pubmed_authors><pubmed_authors>Shi H</pubmed_authors></additional><is_claimable>false</is_claimable><name>HSPB2 facilitates neural regeneration through autophagy for sensorimotor recovery after traumatic brain injury.</name><description>Autophagy is a promising target for promoting neural regeneration, which is essential for sensorimotor recovery following traumatic brain injury (TBI). Whether neuronal heat shock protein B2 (HSPB2), a small molecular heat shock protein, reduces injury and promotes recovery following TBI remains unclear. In this study, we demonstrated that HSPB2 was significantly increased in the neurons of a TBI mouse model, patients, and primary neuron cultures subjected to oxygen/glucose deprivation and reperfusion treatment. Upon creating a tamoxifen-induced neuron-specific HSPB2 overexpression transgenic mouse model, we found that elevated HSPB2 levels promoted long-term sensorimotor recovery and alleviated tissue loss after TBI. We also demonstrated that HSPB2 enhanced white matter structural and fun</description><dates><release>2023-01-01T00:00:00Z</release><publication>2023 Aug</publication><modification>2025-04-22T16:03:13.077Z</modification><creation>2025-04-06T01:33:53.546Z</creation></dates><accession>S-EPMC10543718</accession><cross_references><pubmed>37606039</pubmed><doi>10.1172/jci.insight.168919</doi></cross_references></HashMap>