坏死性下垂
医学
程序性细胞死亡
链脲佐菌素
细胞生物学
内科学
内分泌学
糖尿病
信号转导
细胞凋亡
药理学
生物
生物化学
作者
Pan Gao,Mengying Cao,Xueli Jiang,Xiaolin Wang,Guoping Zhang,Xinru Tang,Chunjie Yang,Issei Komuro,Junbo Ge,Liliang Li,Yunzeng Zou
出处
期刊:Circulation
[Lippincott Williams & Wilkins]
日期:2022-11-30
卷期号:147 (2): 158-174
被引量:47
标识
DOI:10.1161/circulationaha.122.059304
摘要
CB2R transcriptionally repressed necroptosis through interaction with BACH2; in turn, MLKL formed a negative feedback to phosphorylate CB2R. Our study provides the integrative view of a novel molecular mechanism loop for regulation of necroptosis centered by CB2R, which represents a promising alternative strategy for controlling diabetic heart dysfunction.
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