| http://purl.uniprot.org/citations/31990056 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/31990056 | http://www.w3.org/2000/01/rdf-schema#comment | "Apoptosis and fibrosis play a vital role in myocardial infarction (MI) induced tissue injury. Although microRNAs have been the focus of many studies on cardiac apoptosis and fibrosis in MI, the detailed effects of miR-26a is needed to further understood. The present study demonstrated that miR-26a was downregulated in ST-elevation MI (STEMI) patients and oxygen-glucose deprivation (OGD)-treated H9c2 cells. Downregulation of miR-26a was closely correlated with the increased expression of creatine kinase, creatine kinase-MB and troponin I in STEMI patients. Further analysis identified that ataxia-telangiectasia mutated (ATM) was a target gene for miR-26a based on a bioinformatics analysis. miR-26a overexpression effectively reduced ATM expression, apoptosis, and apoptosis-related proteins in OGD-treated H9c2 cells. In a mouse model of MI, the expression of miR-26a was significantly decreased in the infarct zone of the heart, whereas apoptosis and ATM expression were increased. miR-26a overexpression effectively reduced ATM expression and cardiac apoptosis at Day 1 after MI. Furthermore, we demonstrated that overexpression of miR-26a improved cardiac function and reduced cardiac fibrosis by the reduced expression of collagen type I and connective tissue growth factor (CTGF) in mice at Day 14 after MI. Overexpression of miR-26a or ATM knockdown decreased collagen I and CTGF expression in cultured OGD-treated cardiomyocytes. Taken together, these data demonstrate a prominent role for miR-26a in linking ATM expression to ischemia-induced apoptosis and fibrosis, key features of MI progression. miR-26a reduced MI development by affecting ATM expression and could be targeted in the treatment of MI."xsd:string |
| http://purl.uniprot.org/citations/31990056 | http://purl.org/dc/terms/identifier | "doi:10.1002/jcp.29537"xsd:string |
| http://purl.uniprot.org/citations/31990056 | http://purl.uniprot.org/core/author | "Chen Y.L."xsd:string |
| http://purl.uniprot.org/citations/31990056 | http://purl.uniprot.org/core/author | "Chen Y.H."xsd:string |
| http://purl.uniprot.org/citations/31990056 | http://purl.uniprot.org/core/author | "Chen Y.C."xsd:string |
| http://purl.uniprot.org/citations/31990056 | http://purl.uniprot.org/core/author | "Huang C.C."xsd:string |
| http://purl.uniprot.org/citations/31990056 | http://purl.uniprot.org/core/author | "Yang Y.F."xsd:string |
| http://purl.uniprot.org/citations/31990056 | http://purl.uniprot.org/core/author | "Lin M.S."xsd:string |
| http://purl.uniprot.org/citations/31990056 | http://purl.uniprot.org/core/author | "Lee C.W."xsd:string |
| http://purl.uniprot.org/citations/31990056 | http://purl.uniprot.org/core/author | "Chiang M.H."xsd:string |
| http://purl.uniprot.org/citations/31990056 | http://purl.uniprot.org/core/author | "Lin L.C."xsd:string |
| http://purl.uniprot.org/citations/31990056 | http://purl.uniprot.org/core/author | "Liang C.J."xsd:string |
| http://purl.uniprot.org/citations/31990056 | http://purl.uniprot.org/core/author | "Kao H.L."xsd:string |
| http://purl.uniprot.org/citations/31990056 | http://purl.uniprot.org/core/author | "Ke S.R."xsd:string |
| http://purl.uniprot.org/citations/31990056 | http://purl.uniprot.org/core/date | "2020"xsd:gYear |
| http://purl.uniprot.org/citations/31990056 | http://purl.uniprot.org/core/name | "J Cell Physiol"xsd:string |
| http://purl.uniprot.org/citations/31990056 | http://purl.uniprot.org/core/pages | "6085-6102"xsd:string |
| http://purl.uniprot.org/citations/31990056 | http://purl.uniprot.org/core/title | "miR-26a attenuates cardiac apoptosis and fibrosis by targeting ataxia-telangiectasia mutated in myocardial infarction."xsd:string |
| http://purl.uniprot.org/citations/31990056 | http://purl.uniprot.org/core/volume | "235"xsd:string |
| http://purl.uniprot.org/citations/31990056 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/31990056 |
| http://purl.uniprot.org/citations/31990056 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/31990056 |
| http://purl.uniprot.org/uniprot/#_B9EHX4-mappedCitation-31990056 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/31990056 |
| http://purl.uniprot.org/uniprot/#_Q62388-mappedCitation-31990056 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/31990056 |
| http://purl.uniprot.org/uniprot/#_P29268-mappedCitation-31990056 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/31990056 |