{"doi":"10.1016/j.exer.2025.110384","title":"Oxygen uptake at the ocular surface in diabetic animals is impaired in response to central corneal injury","abstract":"Poor wound healing is one of the most devastating complications in late-stage diabetic patients. The avascular cornea does not rely on circulation for its oxygen consumption, uptaking it mainly from the atmosphere. Previous studies demonstrated that oxygen uptake (O 2 U) in diabetic experimental animals and patients is significantly lower than in the non-diabetic condition. Our recent experiments show that upon wounding of the central cornea the O 2 U decreased across the ocular surface, followed by two increases at 6–24 h, and at 72 h, which appeared to be important for proper wound healing. It is however not known whether the two distinct O 2 U increases are maintained in diabetic ocular surface in response to corneal injury. In this study, we used an optic-fiber oxygen micro-sensor to measure O 2 U across the ocular surface of streptozotocin (STZ)- induced diabetic mice and age-matched control mice following injury to the central cornea. We found that the injury causes an immediate and substantial reduction of O 2 U across the ocular surface. O 2 U in non-diabetic corneas increases at 2–6 h post wounding (hpw), decreasing again before the second rise to peak at 72 hpw, especially at the limbus. O 2 U in the diabetic cornea decreases more markedly than that of non-diabetic control. This defective diabetic O 2 U persisted, precluding the two dynamic rises in O 2 U, leading to a failure in recovery. Altogether, our results suggest a previously unknown mechanism of a defective O 2 U response to injury in the diabetic ocular surface, which warrants further research and may lead to new therapeutic paths. Wounding the cornea in vivo caused massive reduction in O 2 uptake (O 2 U) across the ocular surface. O 2 U in non-diabetic corneas showed dynamic changes in O 2 U, increasing 2-6 hours post wounding (hpw), decreasing again before another increase returning to preinjury level at 72 hpw. O 2 U in the diabetic cornea decreased drastically and more significantly than that of non-diabetic control, as the dynamic response of O 2 U was lost. The defective O 2 U kept deteriorating and failed to recover, despite the same and ample O 2 supply, suggesting a previously unknown mechanisms of overall defective responses to injury in O 2 U in diabetic tissues other than vasculopathy that limits blood supply. • A scanning micro-optrode technique measures oxygen uptake (O 2 U) non-invasively. • Wounding cornea results in a massive reduction of O 2 U across the ocular surface. • O 2 U in diabetic corneas decreases more significantly than the non-diabetic control. • O 2 U in diabetic cornea kept dropping, losing its dynamic response, never recovers. • Abnormal O 2 metabolism and vasculopathy may underlying hypoxia in diabetes.","journal":"Experimental Eye Research","year":2025,"id":552312,"datarank":0.0,"base_score":0.0,"endowment":0.0,"self_citation_contribution":0.0,"citation_network_contribution":0.0,"self_endowment_contribution":0.0,"citer_contribution":0.0,"corpus_percentile":null,"corpus_rank":null,"citation_count":1,"citer_count":0,"citers_with_citation_signal":0,"citers_with_endowment":0,"datacite_reuse_total":0,"is_dataset":false,"is_dataset_confidence":0.9559,"is_data_producer":false,"deposit_databanks":null,"is_oa":true,"file_count":0,"downloads":0,"has_version_chain":false,"published_date":"2025-01-01","fair_score":null,"fair_percentile":null,"algorithm_id":"datarank_citation_only_1hop_v6","ranking_scope":"data_only","authors":[{"id":1125075,"name":"Qin Sun","orcid":"0000-0002-7190-6462","position":1,"is_corresponding":false},{"id":1240470,"name":"Li Ma","orcid":"0000-0002-5551-707X","position":2,"is_corresponding":false},{"id":1240469,"name":"Fernando Ferreira","orcid":"0000-0001-5786-8896","position":3,"is_corresponding":false},{"id":561726,"name":"Brian Reid","orcid":"0000-0003-2966-1251","position":4,"is_corresponding":false},{"id":257941,"name":"Min Zhao","orcid":"0000-0002-2500-3035","position":5,"is_corresponding":false},{"id":1355874,"name":"Ana M Sandoval-Castellanos","orcid":"0000-0002-6557-5505","position":0,"is_corresponding":true}],"reference_count":49,"raw_metadata":null,"created_at":"2026-07-19T02:54:33.203144Z","pmid":"40204226","pmcid":null,"fwci":null,"citation_percentile":null,"influential_citations":0,"oa_status":null,"license":null,"views":0,"total_file_size_bytes":0,"version_count":0,"fair_f":null,"fair_a":null,"fair_i":null,"fair_r":null,"fair_zscore":null,"fair_rationale":null,"fair_model":null,"fair_agent_version":null,"fair_fulltext_source":null,"fair_has_llm":null,"fair_computed_at":null,"clinical_trials":[],"software_tools":[],"db_accessions":[],"linked_datasets":[],"topics":[]}