Cellular and molecular mechanisms of endothelial ischemia/reperfusion injury: perspectives and implications for postischemic myocardial protection.
نویسندگان
چکیده
Ischemia/reperfusion (I/R) injury is a major cause of myocardial damage. Despite continuous efforts, minimizing I/R injury still represents a great challenge in standard medical treatments of ischemic heart disease, i.e., thrombolytic therapy, primary percutaneous coronary intervention, and coronary arterial bypass grafting. Development of effective interventions and strategies to prevent or reduce myocardial I/R injury is therefore of great clinical significance. Endothelial dysfunction plays a significant role in myocardial I/R injury, which renders endothelial cells an attractive target for postischemic myocardial protection. The rapidly evolving knowledge of the mechanisms of endothelial I/R injury helps broaden perspective for future development of novel strategies targeting endothelium for alleviating myocardial I/R damage. This review provides a comprehensive summary of the cellular and molecular mechanisms of endothelial I/R injury. Current perspectives and future directions for developing endothelium targeting therapeutics for postischemic myocardial protection are further discussed.
منابع مشابه
Pathophysiology of Ischemia/Reperfusion-induced Myocardial Injury: What We Have Learned From Preconditioning and Postconditioning?
Organ damage after reperfusion of previously viable ischemic tissues is defined as ischemia/reperfusion injury. The pathophysiology of ischemia/reperfusion injury involves cellular effect of ischemia, reactive oxygen species and inflammatory cascade. Protection against ischemia/reperfusion injury may be achieved by preconditioning or postconditioning. In this review, we discuss basic mechan...
متن کاملThe Role of Exercise Preconditioning in Cardioprotection against Ischemia Reperfusion Injury
Cardiovascular diseases are still the main cause of mortality around the world. Therefore, it is essential to develop practical means to reduce their burden. A wealth of evidence supports the role of physical exercise in attenuating many of the risk factors of cardiovascular diseases. Moreover, endurance training warrants protection against myocardial infarction. Exercise, even if performed ...
متن کاملMechanisms of sex differences in TNFR2-mediated cardioprotection.
BACKGROUND TNFR1/TNFR2 signaling may mediate different cellular and molecular responses (injury versus protection) and the balance may be affected by sex hormones. Previous studies have shown that females have improved myocardial functional recovery, TNFR1 signaling resistance, and increased SOCS3 expression after acute ischemia/reperfusion when compared with males. However, it is unknown wheth...
متن کاملSivelestat Attenuates Myocardial Reperfusion Injury during Brief Low Flow Postischemic Infusion
The neutrophil elastase inhibitor sivelestat (ONO-5046) possesses unknown mechanisms of cardioprotection when infused following global ischemia, even in the absence of neutrophils. Since myocardial ischemia-reperfusion injury is strongly associated with endothelial dysfunction and reactive oxygen species (ROS) generation during reperfusion, we have tested the hypothesis that infusion of siveles...
متن کاملInvolvement of CD40-CD40L signaling in postischemic lung injury.
Our studies show that ischemia-reperfusion (I/R) in the isolated rat lung causes retention of lymphocytes, which is associated with increased microvascular permeability, as determined by quantitative measurement of the microvascular filtration coefficient (K(f,c)). Immunoneutralization of either CD40 or CD40L, cell surface proteins important in lymphocyte-endothelial cell proinflammatory events...
متن کاملذخیره در منابع من
با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید
برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید
ثبت ناماگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید
ورودعنوان ژورنال:
- American journal of translational research
دوره 8 2 شماره
صفحات -
تاریخ انتشار 2016