Aortic aneurysm is a focal dilation of the abdominal aorta to a diameter of =30 mm in humans and is mostly asymptomatic, which is associated with a mortality rate of 50% to 80% upon rupture. Although Aortic aneurysm is a well-investigated condition, an available therapy that can tackle constant aneurismal growth is currently lacking. From a clinical perspective, a greater understanding of the genetic and epigenetic mechanisms in depth would allow improved medical therapy to stabilize the aortic wall, which could lead to the prevention of disease progression. Therefore, we want to discuss the potential contribution of genetic and epigenetic mechanisms to aortic aneurysm pathogenesis. Myocardial ischemia-reperfusion injury may cause myocardial stunning, reperfusion arrhythmia, no-reflow phenomenon, and lethal reperfusion injury, which has a significant effect on the prognosis of patients undergoing thrombolytic agent therapy and percutaneous coronary intervention. Ischemia/reperfusion-induced cardiomyocyte injury involves several interrelated factors such as calcium overload and excessive reactive oxygen production leading to cell injury via necrosis, apoptosis, and accelerated autophagy. Therefore, understanding the role and potential mechanisms in the pathogeneses of myocardial ischemia/reperfusion injury may help establish a novel strategy for pharmacologically treating ischemia/reperfusion-induced myocardial injury.
Aortic aneurysm has shown to cluster within certain families and there is evidence showing a strong genetic component in aortic aneurysm risk. From a clinical perspective, a greater understanding of the genetic and epigenetic mechanisms in depth would allow improved medical therapy to stabilize the aortic wall, which could lead to the prevention of disease progression. We want to solve the genetic and epigenetic mechanism of the aneurysm at the specific cellular and molecular level. With the rapid development of bioinformatics, we look forward to finding genetic and epigenetic clues from bioinformatics. This mechanism is best can be verified by clinical and basic experimental. 2. Ischemia-reperfusion injury pathophysiology encompasses many cells including cardiomyocytes, fibroblasts, mesenchymal stromal cells, vascular endothelial and smooth muscle cells, platelets, polymorphonuclear cells, macrophages, and T lymphocytes. Emerging evidence indicates that epigenetic regulation including histone modification, DNA methylation, noncoding RNAs, and N6-methyladenosine (m6A) methylation is closely related to the pathogenesis of myocardial ischemia/reperfusion injury. While the specific mechanisms for all contributing cells and potential molecular pathways are still under investigation.
In this research topic, we will focus on genetic and epigenetic mechanisms involved in the aortic aneurysm or myocardial reperfusion Injury. We welcome submissions of Original Research papers and Reviews focusing on but not limited to:
• Epigenetic modification and myocardial ischemia-reperfusion injury
• Epigenetic regulation and myocardial ischemic preconditioning
• Non-coding RNA-mediated epigenetic modification and myocardial ischemic preconditioning
• RNA-mediated cell communication and myocardial ischemia-reperfusion injury
Aortic aneurysm is a focal dilation of the abdominal aorta to a diameter of =30 mm in humans and is mostly asymptomatic, which is associated with a mortality rate of 50% to 80% upon rupture. Although Aortic aneurysm is a well-investigated condition, an available therapy that can tackle constant aneurismal growth is currently lacking. From a clinical perspective, a greater understanding of the genetic and epigenetic mechanisms in depth would allow improved medical therapy to stabilize the aortic wall, which could lead to the prevention of disease progression. Therefore, we want to discuss the potential contribution of genetic and epigenetic mechanisms to aortic aneurysm pathogenesis. Myocardial ischemia-reperfusion injury may cause myocardial stunning, reperfusion arrhythmia, no-reflow phenomenon, and lethal reperfusion injury, which has a significant effect on the prognosis of patients undergoing thrombolytic agent therapy and percutaneous coronary intervention. Ischemia/reperfusion-induced cardiomyocyte injury involves several interrelated factors such as calcium overload and excessive reactive oxygen production leading to cell injury via necrosis, apoptosis, and accelerated autophagy. Therefore, understanding the role and potential mechanisms in the pathogeneses of myocardial ischemia/reperfusion injury may help establish a novel strategy for pharmacologically treating ischemia/reperfusion-induced myocardial injury.
Aortic aneurysm has shown to cluster within certain families and there is evidence showing a strong genetic component in aortic aneurysm risk. From a clinical perspective, a greater understanding of the genetic and epigenetic mechanisms in depth would allow improved medical therapy to stabilize the aortic wall, which could lead to the prevention of disease progression. We want to solve the genetic and epigenetic mechanism of the aneurysm at the specific cellular and molecular level. With the rapid development of bioinformatics, we look forward to finding genetic and epigenetic clues from bioinformatics. This mechanism is best can be verified by clinical and basic experimental. 2. Ischemia-reperfusion injury pathophysiology encompasses many cells including cardiomyocytes, fibroblasts, mesenchymal stromal cells, vascular endothelial and smooth muscle cells, platelets, polymorphonuclear cells, macrophages, and T lymphocytes. Emerging evidence indicates that epigenetic regulation including histone modification, DNA methylation, noncoding RNAs, and N6-methyladenosine (m6A) methylation is closely related to the pathogenesis of myocardial ischemia/reperfusion injury. While the specific mechanisms for all contributing cells and potential molecular pathways are still under investigation.
In this research topic, we will focus on genetic and epigenetic mechanisms involved in the aortic aneurysm or myocardial reperfusion Injury. We welcome submissions of Original Research papers and Reviews focusing on but not limited to:
• Epigenetic modification and myocardial ischemia-reperfusion injury
• Epigenetic regulation and myocardial ischemic preconditioning
• Non-coding RNA-mediated epigenetic modification and myocardial ischemic preconditioning
• RNA-mediated cell communication and myocardial ischemia-reperfusion injury
