Abstract
Myocardial ischemia and reperfusion injury (MIRI) is a serious complication after percutaneous coronary intervention, which leads to heart failure, increased infarction size, and severe arrhythmias. Various signaling pathways were found to be participated in the process of MIRI, such as phosphatidylinositol 3-kinase (PI3K)/AKT, extracellular signal-regulated kinase (ERK), endothelial NO synthase (eNOS), etc
Highlights
The mechanisms of MIRI is complicated, considering the system is combined with various nonlinear components and frequently exhibit non-intuitive behavior, using the dynamic MIRI model showed in the present study will provide a powerful method to reveal the vague secrets
We used the MIRI model to provide a solve to the interesting question, what is the focus of CaMKII/[Na+]i/[Ca2+]i feedback, which is more important between CaMKII and INa
Our study indicate that CaMKII plays a key role in calcium overload in MIRI, not INa, blocking of CaMKII
Summary
The mechanisms of MIRI is complicated, considering the system is combined with various nonlinear components and frequently exhibit non-intuitive behavior, using the dynamic MIRI model showed in the present study will provide a powerful method to reveal the vague secrets.
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
