ENAGenomicsHongqiao International Institute of Medicine, Tongren Hospital, Shanghai Jiao Tong University School of Medicinehttps://www.ebi.ac.uk/ena/browser/view/PRJEB55091Oxidative stress and cell apoptosis play pivotal roles in the pathogenesis of doxorubicin (DOX)-induced myocardial injury. HSP-17 is a peptide that is lowly expressed in heart tissue from DOX-treated mice. It has a high bioactivity and interspecies sequence consistency, and is predicted to have myocardial protective effects. We have proved that HSP-17 peptide can increase cell viability, protect mitochondrial potential, reduce LDH levels, and reduce ROS and cardiomyocyte apoptosis. To investigate the mechanism underlying cardioprotective role of HSP-17, H9c2 cells were pretreated with 10 μM HSP-17 or scramble peptide for 2 hrs and then insuled by 1 μM DOX for 24 hrs.Total RNA was harvested, and then subjected to quality control and purification. cDNA libraries were created and sequenced on an Illumina HiSeq System.ENAfalseundefinedEffect of HSP-17 peptide on gene expression of doxorubicin-treated H9c2 cells.2022-07-302022-07-30PRJEB55091