Science and Technology Achievement Incubation Center, Kunming Medical University, Kunming, China.
Department of Cardiology, The Second Affiliated Hospital, Kunming Medical University, Kunming, 650032, China.
J Physiol Biochem. 2023 Feb;79(1):47-57. doi: 10.1007/s13105-022-00919-z. Epub 2022 Oct 4.
Acute myocardial infarction (AMI) is a common disease with high morbidity and mortality worldwide. However, postinfarction pathogenesis remains unclear, and it is particularly important to identify new therapeutic targets. The RNA-binding motif protein RBM3 (also known as cold-inducible protein) is known to promote translation and is associated with tumor proliferation and neuroprotection. However, little is known about the biological effects of RBM3 on myocardial infarction. In the present study, we found that RBM3 expression was significantly upregulated in ischemia-reperfusion (I/R) condition and downregulation of RBM3 inhibited autophagy and promoted apoptosis in cardiomyocytes. We confirmed that RBM3 interacts with Raptor to regulate the autophagy pathway. Taken together, these findings illustrate the protective effects of RBM3 against I/R-induced myocardial apoptosis through the autophagy pathway.
急性心肌梗死（AMI）是一种常见疾病，在全球范围内具有较高的发病率和死亡率。然而，梗死后的发病机制仍不清楚，因此确定新的治疗靶点尤为重要。RNA 结合基序蛋白 RBM3（也称为冷诱导蛋白）已知可促进翻译，并与肿瘤增殖和神经保护有关。然而，关于 RBM3 对心肌梗死的生物学影响知之甚少。在本研究中，我们发现 RBM3 的表达在缺血再灌注（I/R）条件下显著上调，下调 RBM3 可抑制自噬并促进心肌细胞凋亡。我们证实 RBM3 与 Raptor 相互作用以调节自噬途径。综上所述，这些发现表明 RBM3 通过自噬途径对 I/R 诱导的心肌细胞凋亡具有保护作用。
