RNA-sequencing analysis gene expression changes of H9C2 treated with CIRBP in response to oxygen-glucose deprivation/reperfusion

Cardiac arrest (CA) represents a significant public health concern, placing a substantial burden on the healthcare system. Post-restoration of autonomous circulation, a majority of patients encounter myocardial dysfunction, a primary cause of death in individuals with cardiac arrest. Hence, the identification of novel therapeutic approaches to enhance myocardial resilience in high-risk cardiac arrest patients holds immense clinical importance. Cold-inducible RNA-binding protein (CIRBP) serves as a vital player in cellular protection and stress resistance, induced by cold conditions. Studies have indicated that the elevation of CIRBP through its agonists can impede the progression of heart failure. However, its role in cardiac toxicity prompted by cardiac arrest remains ambiguous. This study delves into investigating the protective mechanism of CIRBP on cardiac function post-cardiac arrest and sheds light on potential target genes regulated by CIRBP via transcriptome sequencing. Our research outcomes highlight the robust cardioprotective impact of CIRBP on cardiac dysfunction triggered by cardiac arrest and resuscitation.心脏骤停（Cardiac arrest, CA）是一类重大公共卫生问题，给医疗体系带来了沉重负担。自主循环恢复后，多数患者会出现心肌功能障碍，这也是心脏骤停患者死亡的核心诱因之一。因此，开发新型治疗手段以提升高危心脏骤停患者的心肌应激韧性，具备极高的临床研究价值。冷诱导RNA结合蛋白（Cold-inducible RNA-binding protein, CIRBP）是介导细胞保护与应激抵抗的关键因子，可被低温环境诱导表达。已有研究证实，通过激动剂上调CIRBP的表达可延缓心力衰竭的进展。但目前CIRBP在心脏骤停诱发的心肌毒性中的作用仍不明确。本研究深入探讨了CIRBP对心脏骤停后心功能的保护机制，并通过转录组测序阐明了CIRBP所调控的潜在靶基因。本研究结果表明，CIRBP对心脏骤停及复苏诱发的心肌功能障碍具有显著的心脏保护效应。