首页|piRNA DQ725559通过抑制心肌细胞铁死亡通路抗心肌缺血再灌注损伤的作用

piRNA DQ725559通过抑制心肌细胞铁死亡通路抗心肌缺血再灌注损伤的作用

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为探究心肌缺血再灌注损伤(Ischemia-reperfusion Injury,IRI)与铁死亡关系,寻找相关Piwi相互作用RNA(Piwi-interacting RNA,piRNA),利用小鼠乳鼠原代心肌细胞缺氧/复氧(Hypoxia/Reoxygenation,H/R)构建心肌细胞 IRI 模型,通过细胞生存率反映诱导铁死亡最佳 H/R 时间点,筛选铁死亡相关 piRNA,检测铁死亡相关指标变化.研究结果显示,缺氧 18 h/复氧 6 h后,心肌细胞铁死亡和IRI呈现关联,抑制DQ725559 的表达会加重心肌细胞铁死亡和IRI,过表达 DQ725559 会减轻心肌细胞铁死亡和 IRI.研究结果表明,DQ725559 可通过调节心肌细胞铁死亡通路发挥 IRI 调控作用,过表达 DQ725559 可成为RNA治疗心血管疾病新策略.
piRNA DQ725559 Resists Myocardial Ischemia-reperfusion Injury by Inhibiting the Ferroptosis Pathway of Cardiomyocytes
To explore the relationship between myocardial ischemia-reperfusion injury(IRI)and ferropto-sis,and to find related Piwi-interacting RNA(piRNA),myocardial cell IRI model was constructed by Hy-poxia/Reoxygenation(H/R)of primary cardiomyocytes from neonatal mice.The optimal H/R time point for inducing ferroptosis was reflected by cell survival rate.piRNA associated with ferroptosis was screened and changes of ferroptosis related indexes were detected.The results show that ferroptosis is associated with myocardial IRI after hypoxia for 18 h and reoxygenation for 6 h.Inhibition of DQ725559 expression aggravates ferroptosis and myocardial IRI,while overexpression of DQ725559 alleviates ferroptosis and myocardial IRI.This suggests that DQ725559 can play a role in the regulation of myocardial IRI by regula-ting the ferroptosis pathway of cardiomyocytes,and overexpression of DQ725559 could be a new strategy for RNA therapy of cardiovascular diseases.

ischemia-reperfusion injurypiRNAcardiomyocytesferroptosis

王瑞荃、陈鑫哲、王涛、王昆

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青岛大学转化医学研究院,青岛 266021

缺血再灌注损伤 piRNA 心肌细胞 铁死亡

国家自然科学基金

82070313

2024

青岛大学学报(自然科学版)
青岛大学

青岛大学学报(自然科学版)

影响因子:0.248
ISSN:1006-1037
年,卷(期):2024.37(1)
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