Circulation：瑞金医院闫小响团队发现心肌肥厚和心力衰竭关键驱动信号

2022-04-03 MedSci原创 MedSci原创发表于威斯康星

上海交通大学医学院附属瑞金医院心脏内科闫小响教授研究团队在心肌能量代谢调控心力衰竭的发生发展方面取得新进展，研究成果以“DYRK1B-STAT3通过抑制线粒体能量代谢驱动心肌肥厚和心力衰竭

上海交通大学医学院附属瑞金医院心脏内科闫小响教授研究团队在心肌能量代谢调控心力衰竭的发生发展方面取得新进展，研究成果以“DYRK1B-STAT3通过抑制线粒体能量代谢驱动心肌肥厚和心力衰竭进展（DYRK1B-STAT3 drives cardiac hypertrophy and heart failure by impairing mitochondrial bioenergetics）”为题，于2022年3月3日在《循环》（Circulation）杂志上在线发表。

心力衰竭是各种心脏疾病的终末阶段，尽管规范化治疗能改善心衰患者的临床症状，并降低了主要心血管事件的发生，但治疗心力衰竭仍是临床面临的一个难题。因此，深入探索心衰发生过程中的机制和干预靶点，进一步改善患者的远期预后具有重要意义。

研究表明，蛋白激酶系统在心肌能量代谢障碍致心力衰竭的发生中发挥重要作用。闫小响研究团队通过DYRK1B心脏特异性转基因和敲除小鼠，发现DYRK1B过表达直接导致自发性心力衰竭；而DYRK1B敲除明显抑制TAC诱导的心肌肥厚和心力衰竭。

DYRK1B overexpression results in heart failure.

并揭示DYRK1B通过与STAT3结合，促进其705位点的磷酸化和细胞核内聚集，进而负向调控心肌组织中PGC-1α的表达，最终导致心肌细胞线粒体能量生成障碍和心力衰竭的发生。

DYRK1B deletion attenuates TAC-indued cardiac hypertrophy and heart failure.

为推动该成果的临床转化，团队分别使用DYRK1B抑制剂和STAT3抑制剂探究其潜在临床应用价值，发现STAT3抑制剂（S31-201）能够显著减轻DYRK1B过表达引起的线粒体能量代谢受损和心功能不全，而DYRK1B抑制剂（AZ191）减轻TAC手术引起的STAT3激活、线粒体能量受损和心室肥厚。

DYRK1B drives cardiac dysfunction by impairing mitochondrial bioenergetics.

研究证明DYRK1B-STAT3信号轴通过抑制PGC-1α的表达致线粒体能量代谢受损，进而参与心力衰竭的发生，为调控心肌细胞能量代谢防治心力衰竭提供新的理论支持。

STAT3 inhibition rescues DYRK1B overexpression-induced heart failure.

图 DYRK1B调控心肌线粒体能量代谢参与心力衰竭的机制示意图

原始出处：

Zhuang L, Jia K, Chen C, Li Z, Zhao J, Hu J, Zhang H, Fan Q, Huang C, Xie H, Lu L, Shen W, Ning G, Wang J, Zhang R, Chen K, Yan X.DYRK1B-STAT3 Drives Cardiac Hypertrophy and Heart Failure by Impairing Mitochondrial Bioenergetics.Circulation. 2022 Mar 15;145(11):829-846

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2022-05-05 148a60abm39暂无昵称

学习了

58 0
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2022-04-04 test-rml

厉害厉害👍

0 0
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2022-04-04 最黄的大芒果

签到

81 0
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2022-04-04 1212ba38m22暂无昵称

学习了

79 0
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2022-04-04 学医无涯

学习一下

87 0
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2022-04-03 医者仁者

厉害！！#心肌肥厚#，可能成为治疗靶点吧

106 0
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2022-04-03 jiangying28

签到

53 0

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