![]() The Janus kinase (JAK) and signal transducer and activator of transcription (STATs) pathway plays critical roles in orchestrating immunity and cell death. ![]() Although IL-17A is not expressed in cardiomyocytes, cardiomyocyte apoptosis is caused by macrophages and neutrophils released IL-17A via IL-17RA during I/R injury. Recently, emerging evidence has indicated that interleukin-17A (IL-17A) induces cardiomyocyte apoptosis by its ubiquitous receptor, IL-17RA, during myocardial I/R injury. Unfortunately, reperfusion therapy unpredictably leads to sterile inflammation and cell death in the myocardium, causing tremendous cardiac injury. The high mortality rate of myocardial infarction has become an important health challenge, particularly taking into consideration that the rapid restoration of coronary flow even leads to salvage of remaining cardiomyocytes after a heart attack. Our results indicate that IL-1R2 protects cardiomyocytes from apoptosis, which provides a therapeutic approach to turn down myocardial I/R injury. Additionally, IL-1R2 overexpression in cardiomyocyte protected cardiomyocyte against apoptosis through reducing the IL-17RA expression both in vivo and in vitro. Consistently, IL-1R2-deficient mice increased immune cells infiltrating into heart after surgery, which was relevant with cardiac damage. Following exposure to hypoxia and reoxygenation (H/R), neonatal rat ventricular myocytes (NRVM) significantly increased IL-1R2 expression relying on NF-κB activation. In addition, IL-1R2-deficient mice heart showed enlarged infarct size, increased cardiomyocyte apoptosis together with reduced cardiac systolic function. Similarly, after myocardial I/R surgery, IL-1R2 expression was significantly increased in heart of wild-type mice. Here we found that the serum levels of IL-1R2 were significantly increased in patients with acute myocardial infarction (AMI) following interventional therapy. However, its role in I/R injury remains unknown. As a decoy receptor of IL-1β, Interleukin-1 receptor type 2 (IL-1R2) inhibits IL-1β signaling. Myocardial ischemia reperfusion (I/R) injury is a complex process with intense inflammatory response and cardiomyocyte apoptosis.
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