<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Lu P</submitter><funding>Winfast Charity Foundation Project</funding><funding>the Natural Science Foundation of Jiangsu Province for Young Scholars, China</funding><funding>National Natural Science Foundation of China</funding><funding>Research Talent Cultivation Project of Zhongda Hospital Southeast Universtiy</funding><funding>Jiangsu Provincial Medical Talent, The Project of Invigorating Health Care through Science, Technology and Education</funding><funding>Natural Science Foundation of Jiangsu Province</funding><pagination>56</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC12849074</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>21(1)</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>Tendinopathy is a common musculoskeletal disorder in individuals with diabetes. Tendon stem/progenitor cells (TSPCs) play an essential role in tendon repair, regeneration and homeostasis maintenance. Although studies have demonstrated that diabetic tendinopathy is closely associated with the altered differentiation of TSPCs, the underlying mechanisms remain largely unknown. This study was designed to investigate the role of the HMGB1/RAGE/β-catenin axis in the differentiation imbalance of TSPCs and diabetic tendinopathy.&lt;h4>Methods&lt;/h4>Rat diabetes models were induced with streptozotocin (65 mg/kg). TSPCs were isolated at week 2 and the patellar tendons were isolated at weeks 2 and 4 for histological analysis. The activation of the HMGB1/RAGE/β-catenin axis in TSPCs and </pubmed_abstract><journal>Journal of orthopaedic surgery and research</journal><pubmed_title>The HMGB1/RAGE/β-catenin axis mediates aberrant osteogenic-tenogenic differentiation imbalance of tendon stem/progenitor cells in diabetic tendinopathy.</pubmed_title><pmcid>PMC12849074</pmcid><funding_grant_id>YL20220525</funding_grant_id><funding_grant_id>CZXM-GSP-RC48</funding_grant_id><funding_grant_id>ZDRCA2016083</funding_grant_id><funding_grant_id>BK20200398</funding_grant_id><funding_grant_id>81572187</funding_grant_id><funding_grant_id>BK20221462</funding_grant_id><pubmed_authors>Shi L</pubmed_authors><pubmed_authors>Li Y</pubmed_authors><pubmed_authors>Rui Y</pubmed_authors><pubmed_authors>Gao Y</pubmed_authors><pubmed_authors>Wang H</pubmed_authors><pubmed_authors>Lu P</pubmed_authors></additional><is_claimable>false</is_claimable><name>The HMGB1/RAGE/β-catenin axis mediates aberrant osteogenic-tenogenic differentiation imbalance of tendon stem/progenitor cells in diabetic tendinopathy.</name><description>&lt;h4>Background&lt;/h4>Tendinopathy is a common musculoskeletal disorder in individuals with diabetes. Tendon stem/progenitor cells (TSPCs) play an essential role in tendon repair, regeneration and homeostasis maintenance. Although studies have demonstrated that diabetic tendinopathy is closely associated with the altered differentiation of TSPCs, the underlying mechanisms remain largely unknown. This study was designed to investigate the role of the HMGB1/RAGE/β-catenin axis in the differentiation imbalance of TSPCs and diabetic tendinopathy.&lt;h4>Methods&lt;/h4>Rat diabetes models were induced with streptozotocin (65 mg/kg). TSPCs were isolated at week 2 and the patellar tendons were isolated at weeks 2 and 4 for histological analysis. The activation of the HMGB1/RAGE/β-catenin axis in TSPCs and </description><dates><release>2025-01-01T00:00:00Z</release><publication>2025 Dec</publication><modification>2026-06-09T05:41:41.581Z</modification><creation>2026-06-09T03:07:46.277Z</creation></dates><accession>S-EPMC12849074</accession><cross_references><pubmed>41444655</pubmed><doi>10.1186/s13018-025-06572-8</doi></cross_references></HashMap>