Cardiovascular disease has been a major threat to human’s health and lives for many years. It is of great importance to explore the mechanisms and develop strategies to prevent the pathogenesis. Generally, cardiovascular disease is associated with endothelial dysfunction, which is closely related to the nitric oxide (NO)mediated vasodilatation. The release of NO is regulated by NOS3 gene in mammals’ vascular system. A great deal of evidences have shown that the polymorphism and epigenetic of NOS3 gene play vital roles in the pathological process of cardiovascular disease. To gain insights into the role of NOS3 in the cardiovascular diseases, we reviewed the molecular mechanisms underlying the development of cardiovascular diseases in this paper, including the uncoupling of NOS3 protein, epigenetic and polymorphism of NOS3 gene. The review can also offer possible strategies to prevent and treat cardiovascular diseases.
ObjectiveTo summarize the therapeutic targets of pancreatic cancer (PC). MethodsThe related literatures about the therapeutic targets of PC were reviewed. ResultsPC was one of the most challenging tumor in worldwide, and was characterized as a highly aggressive disease with poor overall prognosis and a high mortality rate. The hallmark of PC was its poor response to radio-and chemo-therapy. Current chemotherapeutic regimens could not provide substantial survival benefit with a clear increase in overall survival. Recently, several new approaches which could significantly improve the clinical outcome of PC had been described, involving signal-transduction pathways, immune response, stroma reaction, and epigenetic changes. ConclusionsMany therapeutic targets are involved in the treatment of PC. As current therapies failed to significantly improve the progression and the survival of PC, new therapeutic approaches and clinical studies are strongly required.
Recent advances in epigenetics indicate that several epigenetic modifications, including acetylation, methylatio, and microRNA (miRNA), play an important role in the pathogenesis of acute kidney injury (AKI). Our study reveales that enhancement of protein acetylation by pharmacological inhibition of class I histone deacetylases leads to more severe tubular injury, and delays the restoration of renal structure and function. The changes in promoter DNA methylation occurs in the kidney with ischemia/reperfusion. MiRNA expression is associated with the regulation of both renal injury and regeneration after AKI. Targeting the epigenetic process may provide a therapeutic treatment for patients with AKI. The purpose of this review is to summarize recent advances in epigenetic regulation of AKI and provide mechanistic insight into the role of acetylation, methylation, and miRNA expression in the pathological processes of AKI.
ObjectiveTo analyze effects of histone demethylase Jumonji-domaincontaining protein 3 (JMJD3) in macrophages in order to provide a new target for treatment of macrophage-related inflammatory reactions, autoimmune diseases, and organ transplantation rejection.MethodThe related literatures of researches on the effects of JMJD3 in the macrophages in recent years were searched and reviewed.ResultsThe macrophages played the important roles in maintaining tissue homeostasis and host response, clearing pathogens and apoptotic cells, and promoting tissue repair and wound healing. The JMJD3 could regulate the balance of M1 and M2 types of macrophages through the different ways and had different effects on the polarization of M2 macrophages when it was stimulated by the different extracellular substances. In some immune diseases and wound repairing, the JMJD3 could not only promote the inflammatory responses, but also polarize the M2 macrophages so as to inhibit the inflammation and promote the tissue repair. Clinically, the JMJD3 expression might be different in the different diseases and its low or high expression both might be involved in the occurrence of diseases.ConclusionHistone demethylase enzyme JMJD3 is involved in macrophage polarization and expression of inflammatory genes, but there are still many problems that require further to be investigated.
Epigenetics refers to heritable changes in gene expression independent of DNA nucleotide sequence itself, and the main mechanisms include DNA methylation, histone modifications, noncoding RNAs, and so on. Vascular disease is a chronic disease regulated by the interaction between environmental and genetic factors. In recent years, more and more studies have confirmed that epigenetic regulation plays an important role in the occurrence and development of vascular diseases. This article reviews recent advances in epigenetics in vascular disease.
ObjectiveTo summarize the current research status of the relationship between DNA methylation and liver regeneration.MethodThe related literatures at home and abroad were searched to review the studies on relationships between the methylation level of liver cells, regulation of gene expression, and methylation related proteins and liver regeneration.ResultsThe DNA methylation was an important epigenetic regulation method in vivo and its role in the liver regeneration had been paid more and more attentions in recent years. The existing studies had found the epigenetic phenomena during the liver regeneration such as the genomic hypomethylation, methylation changes of related proliferating genes and DNA methyltransferase and UHRF1 regulation of the liver regeneration.ConclusionsThere are many relationships between DNA methylation and liver regeneration. Regulation of liver regeneration from DNA methylation level is expected to become a reality in the near future.