南方科技大学知识苑(SUSTech KC): ANGPTL2 aggravates LPS-induced septic cardiomyopathy via NLRP3-mediated inflammasome in a DUSP1-dependent pathway

题名	ANGPTL2 aggravates LPS-induced septic cardiomyopathy via NLRP3-mediated inflammasome in a DUSP1-dependent pathway
作者	Li, Jun 1,2; Wan, Ting 3; Liu, Cheng 4,5 ; Liu, Huadong 4,5; Ke, Dong 6; Li, Luocheng 7
通讯作者	Ke, Dong; Li, Luocheng
发表日期	2023-10-01
DOI	10.1016/j.intimp.2023.110701
发表期刊	INTERNATIONAL IMMUNOPHARMACOLOGY 影响因子和分区
ISSN	1567-5769
EISSN	1878-1705
卷号	123
摘要	Angiopoietin-like protein 2 (ANGPTL2) was implicated in various cardiovascular diseases; however, its role in lipopolysaccharide (LPS)-related septic cardiomyopathy remains unclear. Herein, mice were exposed to LPS to generate septic cardiomyopathy, and adeno-associated viral vector was employed to overexpress ANGPTL2 in the myocardium. Besides, mice were treated with adenoviral vector to knock down ANGPTL2 in hearts. ANGPTL2 expressions in hearts and cardiomyocytes were upregulated by LPS challenge. ANGPTL2 overexpression aggravated, while ANGPTL2 silence ameliorated LPS-associated cardiac impairment and inflammation. Mechanically, we found that ANGPTL2 activated NLRP3 inflammasome via suppressing DUSP1 signaling, and NLRP3 knockdown abrogated the detrimental role of ANGPTL2 in aggravating LPS-induced cardiac inflammation. Furthermore, DUSP1 overexpression significantly inhibited ANGPTL2-mediated NLRP3 activation, and subsequently improved LPS-related cardiac dysfunction. In summary, ANGPTL2 exacerbated septic cardiomyopathy via activating NLRP3-mediated inflammation in a DUSP1-dependent manner, and our study uncovered a promising therapeutic target in preventing septic cardiomyopathy.
关键词	Heart failure Sepsis Inflammation ANGPTL2 DUSP1
相关链接	[来源记录]
收录类别	SCI
语种	英语
学校署名	其他
WOS研究方向	Immunology ; Pharmacology & Pharmacy
WOS类目	Immunology ; Pharmacology & Pharmacy
WOS记录号	WOS:001052581400001
出版者	ELSEVIER
ESI学科分类	PHARMACOLOGY & TOXICOLOGY
来源库	Web of Science
引用统计	被引频次[WOS]：5
成果类型	期刊论文
条目标识符	http://sustech.caswiz.com/handle/2SGJ60CL/553435
专题	南方科技大学第一附属医院
作者单位	1.Wuhan Univ, Renmin Hosp, Dept Cardiol, Wuhan 430060, Hubei, Peoples R China 2.Wuhan Univ, Cardiovasc Res Inst, Wuhan 430060, Hubei, Peoples R China 3.Wuhan Univ, Renmin Hosp, Dept Gynecol, Wuhan 430060, Hubei, Peoples R China 4.Southern Univ Sci & Technol, Jinan Univ, Shenzhen Peoples Hosp, Affiliated Hosp 1,Clin Med Coll 2,Dept Cardiol,, Shenzhen 518020, Guangdong, Peoples R China 5.Shenzhen Cardiovasc Minimally Invas Med Engn Techn, Shenzhen 518020, Guangdong, Peoples R China 6.Wuhan Univ, Renmin Hosp, Dept Gastrointestinal Surg, Wuhan 430060, Hubei, Peoples R China 7.Wuhan Univ, Renmin Hosp, Dept Cardiovasc Surg, Wuhan 430060, Hubei, Peoples R China
推荐引用方式 GB/T 7714	Li, Jun,Wan, Ting,Liu, Cheng,et al. ANGPTL2 aggravates LPS-induced septic cardiomyopathy via NLRP3-mediated inflammasome in a DUSP1-dependent pathway[J]. INTERNATIONAL IMMUNOPHARMACOLOGY,2023,123.
APA	Li, Jun,Wan, Ting,Liu, Cheng,Liu, Huadong,Ke, Dong,&Li, Luocheng.(2023).ANGPTL2 aggravates LPS-induced septic cardiomyopathy via NLRP3-mediated inflammasome in a DUSP1-dependent pathway.INTERNATIONAL IMMUNOPHARMACOLOGY,123.
MLA	Li, Jun,et al."ANGPTL2 aggravates LPS-induced septic cardiomyopathy via NLRP3-mediated inflammasome in a DUSP1-dependent pathway".INTERNATIONAL IMMUNOPHARMACOLOGY 123(2023).