{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["10(20)"],"submitter":["Chen L"],"pubmed_abstract":["<h4>Background</h4>Ferroptosis, a newly discovered form of cell death, can accumulation activates lipid peroxidation and excessive oxidative stress in a high glucose environment. These phenomena suggest there may be ferroptosis pathways in the pathological processes associated with diabetic ulcer (DU). Platelet-rich plasma (PRP) promotes the healing of DU wounds, which may be achieved by the regulation of ferroptosis pathways. Hence, the present study aimed to investigate this association and uncover the potential underlying mechanisms.<h4>Methods</h4>Cell injury models induced by high glucose were constructed using EA.HY926 (vascular endothelial cells), HSF (fibroblasts), and rat DU models. The MDA, total ROS, total SOD content, the gene and protein expression of <i>GPX4</i>, <i>SLC7A11</"],"journal":["Annals of translational medicine"],"pagination":["1121"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9652541"],"repository":["biostudies-literature"],"pubmed_title":["Platelet-rich plasma promotes diabetic ulcer repair through inhibition of ferroptosis."],"pmcid":["PMC9652541"],"pubmed_authors":["Zhou L","Chen L","Wu D","Ye Y"],"additional_accession":[]},"is_claimable":false,"name":"Platelet-rich plasma promotes diabetic ulcer repair through inhibition of ferroptosis.","description":"<h4>Background</h4>Ferroptosis, a newly discovered form of cell death, can accumulation activates lipid peroxidation and excessive oxidative stress in a high glucose environment. These phenomena suggest there may be ferroptosis pathways in the pathological processes associated with diabetic ulcer (DU). Platelet-rich plasma (PRP) promotes the healing of DU wounds, which may be achieved by the regulation of ferroptosis pathways. Hence, the present study aimed to investigate this association and uncover the potential underlying mechanisms.<h4>Methods</h4>Cell injury models induced by high glucose were constructed using EA.HY926 (vascular endothelial cells), HSF (fibroblasts), and rat DU models. The MDA, total ROS, total SOD content, the gene and protein expression of <i>GPX4</i>, <i>SLC7A11</","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Oct","modification":"2025-04-25T23:34:52.134Z","creation":"2025-04-06T09:26:30.419Z"},"accession":"S-EPMC9652541","cross_references":{"pubmed":["36388823"],"doi":["10.21037/atm-22-4654"]}}