{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Chen Y"],"funding":["Natural Science Foundation of Shanghai","National Natural Science Foundation of China","Shanghai Pujiang Program"],"pagination":["100"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11909899"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["31(1)"],"pubmed_abstract":["Background
Acute myocardial infarction (AMI) is a leading cause of mortality, characterized by myocardial ischemia that induces cardiomyocyte apoptosis and subsequent cardiac dysfunction. Sirtuin 1 (Sirt1) has emerged as a key regulator of cell survival and apoptosis, particularly under hypoxic conditions.Methods
An AMI animal model was established via ligation of the left anterior descending (LAD) coronary artery. Gene expression in the infarcted region was evaluated at various time points. Sirt1 overexpression and control lentivirus were administered to the peri-infarct region of mice heart. After LAD ligation, assessment on myocardial infarct size, cardiac function, and cardiomyocyte apoptosis were performed. In vitro, primary mouse cardiomyocytes subjected to hypoxia we"],"journal":["Molecular medicine (Cambridge, Mass.)"],"pubmed_title":["Sirtuin1 mitigates hypoxia-induced cardiomyocyte apoptosis in myocardial infarction via PHD3/HIF-1α."],"pmcid":["PMC11909899"],"funding_grant_id":["82070401, 81800339 and 81700394","19ZR1443400","22PJD044"],"pubmed_authors":["Chen J","Yang K","Wu Q","Cao J","Xue Q","Ren Y","Chen Y","Shan S"],"additional_accession":[]},"is_claimable":false,"name":"Sirtuin1 mitigates hypoxia-induced cardiomyocyte apoptosis in myocardial infarction via PHD3/HIF-1α.","description":"Background
Acute myocardial infarction (AMI) is a leading cause of mortality, characterized by myocardial ischemia that induces cardiomyocyte apoptosis and subsequent cardiac dysfunction. Sirtuin 1 (Sirt1) has emerged as a key regulator of cell survival and apoptosis, particularly under hypoxic conditions.Methods
An AMI animal model was established via ligation of the left anterior descending (LAD) coronary artery. Gene expression in the infarcted region was evaluated at various time points. Sirt1 overexpression and control lentivirus were administered to the peri-infarct region of mice heart. After LAD ligation, assessment on myocardial infarct size, cardiac function, and cardiomyocyte apoptosis were performed. In vitro, primary mouse cardiomyocytes subjected to hypoxia we","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Mar","modification":"2025-04-18T12:50:29.012Z","creation":"2025-04-06T22:13:29.058Z"},"accession":"S-EPMC11909899","cross_references":{"pubmed":["40087582"],"doi":["10.1186/s10020-025-01155-z"]}}