{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Bi F"],"funding":["Natural Science Foundation of Xiamen Municipality","National Natural Science Foundation of China","Harbin Medical University","Department of Education, Fujian Province"],"pagination":["114810"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12924730"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["29(3)"],"pubmed_abstract":["Angiogenesis is essential for myocardial repair after myocardial infarction (MI). While Y-box binding protein 1 (YBX1) is well-established in cancer biology, its role in post-MI angiogenesis remains unknown. Here, we show that YBX1 expression is increased in endothelial cells after MI, with higher levels observed in the peri-infarct region, and is also induced in hypoxic HUVECs. <i>In vitro</i>, YBX1 overexpression enhances HUVEC viability, migration, and proliferation, whereas siRNA-mediated knockdown impairs these functions. <i>In vivo</i>, endothelial-specific AAV9-YBX1 delivery improves cardiac function, reduces fibrosis, and enhances angiogenesis in murine MI models, while AAV9-shYBX1 exacerbates cardiac injury. Mechanistically, RNA sequencing reveals that YBX1 deficiency disrupts HIF"],"journal":["iScience"],"pubmed_title":["YBX1 promotes angiogenesis after myocardial infarction by stabilizing HIF1α mRNA via m&lt;sup&gt;6&lt;/sup&gt;A signaling."],"pmcid":["PMC12924730"],"funding_grant_id":["82470248","HYDYYXQN202405","210482","82170299","3502Z202373125"],"pubmed_authors":["Liu H","Cao M","Li J","Shan H","Tian H","Wang H","Kong C","Zhou Y","Bi F","He Y","Xiao H","Yu T","Liu F","Wu Y"],"additional_accession":[]},"is_claimable":false,"name":"YBX1 promotes angiogenesis after myocardial infarction by stabilizing HIF1α mRNA via m&lt;sup&gt;6&lt;/sup&gt;A signaling.","description":"Angiogenesis is essential for myocardial repair after myocardial infarction (MI). While Y-box binding protein 1 (YBX1) is well-established in cancer biology, its role in post-MI angiogenesis remains unknown. Here, we show that YBX1 expression is increased in endothelial cells after MI, with higher levels observed in the peri-infarct region, and is also induced in hypoxic HUVECs. <i>In vitro</i>, YBX1 overexpression enhances HUVEC viability, migration, and proliferation, whereas siRNA-mediated knockdown impairs these functions. <i>In vivo</i>, endothelial-specific AAV9-YBX1 delivery improves cardiac function, reduces fibrosis, and enhances angiogenesis in murine MI models, while AAV9-shYBX1 exacerbates cardiac injury. Mechanistically, RNA sequencing reveals that YBX1 deficiency disrupts HIF","dates":{"release":"2026-01-01T00:00:00Z","publication":"2026 Mar","modification":"2026-07-16T18:48:29.069Z","creation":"2026-07-12T03:08:35.763Z"},"accession":"S-EPMC12924730","cross_references":{"pubmed":["41732278"],"doi":["10.1016/j.isci.2026.114810"]}}