Roles of IL-33 in the Pathogenesis of Cardiac Disorders

被引:6
作者
Jiang, Chunjie [1 ]
Jin, Xuemei [1 ,2 ]
Li, Chunlei [1 ]
Wen, Luona [1 ]
Wang, Yuqi [1 ]
Li, Xiaojian [3 ]
Zhang, Zhi [3 ]
Tan, Rongshao [1 ]
机构
[1] Jinan Univ, Guangzhou Inst Dis Oriented Nutr Res, Dept Clin Nutr, Guangzhou Red Cross Hosp, Guangzhou 510220, Peoples R China
[2] Yanbian Univ, Sch Med, Dept Prevent Med, Yanji 133002, Peoples R China
[3] Jinan Univ, Guangzhou Red Cross Hosp, Dept Burns, Guangzhou 510220, Peoples R China
关键词
IL-33; heart transplantation; hypertensive heart disease; myocardial infarction; coronary atherosclerotic heart disease; diabetic cardiomyopathy; HEART-FAILURE; ST2; RECEPTOR; SERUM-LEVELS; INTERLEUKIN-33; CELLS; CYTOKINE; INFLAMMATION; PROTEIN; MYOCARDITIS; SIGNALS;
D O I
10.1177/15353702231198075
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Interleukin-33 (IL-33) is a member of the IL-1 cytokine family and is believed to play important roles in different diseases by binding to its specific receptor suppression of tumorigenicity 2 (ST2). In the heart, IL-33 is expressed in different cells including cardiomyocytes, fibroblasts, endothelium, and epithelium. Although many studies have been devoted to investigating the effects of IL-33 on heart diseases, its roles in myocardial injuries remain obscure, and thus further studies are mandatory to unravel the underlying molecular mechanisms. We highlighted the current knowledge of the molecular and cellular characteristics of IL-33 and then summarized its major roles in different myocardial injuries, mainly focusing on infection, heart transplantation, coronary atherosclerosis, myocardial infarction, and diabetic cardiomyopathy. This narrative review will summarize current understanding and insights regarding the implications of IL-33 in cardiac diseases and its diagnostic and therapeutic potential for cardiac disease management.
引用
收藏
页码:2167 / 2174
页数:8
相关论文
共 76 条
[1]   Th2 Regulation of Viral Myocarditis in Mice: Different Roles for TLR3 versus TRIF in Progression to Chronic Disease [J].
Abston, Eric D. ;
Coronado, Michael J. ;
Bucek, Adriana ;
Bedja, Djahida ;
Shin, Jaewook ;
Kim, Joseph B. ;
Kim, Eunyong ;
Gabrielson, Kathleen L. ;
Georgakopoulos, Dimitrios ;
Mitzner, Wayne ;
Fairweather, DeLisa .
CLINICAL & DEVELOPMENTAL IMMUNOLOGY, 2012,
[2]  
Aimo A., 2018, INT J CARDIOL, V267
[3]   Angiotensin Converting Enzyme Inhibitors (ACEIs) Decrease the Progression of Cardiac Fibrosis in Rheumatic Heart Disease Through the Inhibition of IL-33/sST2 [J].
Ambari, Ade M. ;
Setianto, Budhi ;
Santoso, Anwar ;
Radi, Basuni ;
Dwiputra, Bambang ;
Susilowati, Eliana ;
Tulrahmi, Fadilla ;
Doevendans, Pieter A. ;
Cramer, Maarten J. .
FRONTIERS IN CARDIOVASCULAR MEDICINE, 2020, 7
[4]   Molecular characterization of NF-HEV, a nuclear factor preferentially expressed in human high endothelial venules [J].
Baekkevold, ES ;
Roussigné, M ;
Yamanaka, T ;
Johansen, FE ;
Jahnsen, FL ;
Amalric, F ;
Brandtzaeg, P ;
Erard, M ;
Haraldsen, G ;
Girard, JP .
AMERICAN JOURNAL OF PATHOLOGY, 2003, 163 (01) :69-79
[5]   The Reparative Roles of IL-33 [J].
Bou Saba, Johnny ;
Turnquist, Heth R. .
TRANSPLANTATION, 2023, 107 (05) :1069-1078
[6]   Interleukin-33 prolongs allograft survival during chronic cardiac rejection [J].
Brunner, Stefan M. ;
Schiechl, Gabriela ;
Falk, Werner ;
Schlitt, Hans J. ;
Geissler, Edward K. ;
Fichtner-Feigl, Stefan .
TRANSPLANT INTERNATIONAL, 2011, 24 (10) :1027-1039
[7]   IL-33, the IL-1-like cytokine ligand for ST2 receptor, is a chromatin-associated nuclear factor in vivo [J].
Carriere, Virginie ;
Roussel, Lucie ;
Ortega, Nathalie ;
Lacorre, Delphine-Armelle ;
Americh, Laure ;
Aguilar, Luc ;
Bouche, Gerard ;
Girard, Jean-Philippe .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2007, 104 (01) :282-287
[8]   Interleukin-33 (IL-33): A nuclear cytokine from the IL-1 family [J].
Cayrol, Corinne ;
Girard, Jean-Philippe .
IMMUNOLOGICAL REVIEWS, 2018, 281 (01) :154-168
[9]   Eplerenone Modulates Interleukin-33/sST2 Signaling and IL-1 in Left Ventricular Systolic Dysfunction After Acute Myocardial Infarction [J].
Chen, Bo ;
Geng, Jing ;
Gao, Shao-Xi ;
Yue, Wen-Wei ;
Liu, Qiang .
JOURNAL OF INTERFERON AND CYTOKINE RESEARCH, 2018, 38 (03) :137-144
[10]   Myocardial pressure overload induces systemic inflammation through endothelial cell IL-33 [J].
Chen, Wei-Yu ;
Hong, Jaewoo ;
Gannon, Joseph ;
Kakkar, Rahul ;
Lee, Richard T. .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2015, 112 (23) :7249-7254