Abstract
Objectives: Myocardial injury caused by ischemia followed by reperfusion mediates a complex series of inflammatory response that reduces the benefit of medical interventions, such as percutaneous coronary intervention, thrombolytic therapy, and coronary bypass surgery. Therefore, suppression of Ischemia/Reperfusion (I/R) -mediated myocardial injury is important in clinical practice. The objective of this study was to investigate whether vitamin has some protective effect on heart after myocardial I/R, and the mechanistic pathway of this effect.
Highlights
Ischemic heart disease is the most common of human disability and unless the previous trends are changed, it will continue to be the most common cause of death in 2030. [1] Ischemia and Reperfusion (I/R) injury, a general healthy problem, is due to the restoration of blood after the time of coronary artery impaired
We determined whether Vit D improved cardiac function in mice following I/R
The resulting data showed that significantly greater reduction in the plasma level of cardiac Troponin-I (cTn-I) reflected the potential role of Vitamin D (vit D) in decreased cardiac injurys following I/R as shown in (Fig. 1b)
Summary
Ischemic heart disease is the most common of human disability and unless the previous trends are changed, it will continue to be the most common cause of death in 2030. [1] Ischemia and Reperfusion (I/R) injury, a general healthy problem, is due to the restoration of blood after the time of coronary artery impaired. [1] Ischemia and Reperfusion (I/R) injury, a general healthy problem, is due to the restoration of blood after the time of coronary artery impaired. The restorations flow of blood supply to an ischemic heart refers to myocardial reperfusion which induced myocardial injury [4]. Reperfusion of ischemic tissue results in a local and a systemic inflammatory response that may result in wide range of microvascular dysfunction and changing in tissue barrier function [5]. Other studies showed that the activation of ERK can mediate cell death depending on the stimuli and cell types involved. To understanding the mechanistic pathway of Vitamin D following I/R, we tested the hypothesis that vit D improved cardiac function after I/R through downregulation of ERK1/2 pathway
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