About this Research Topic
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
Keywords: Genetic modulation, Epigenetic regulation, Myocardial reperfusion injury
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