lincRNA-ROR通过miR-145-ZEB2调控HERC5介导的p53蛋白ISG化修饰在肝纤维化中的作用及机制研究
糖水鸡蛋摘要：
肝纤维化是慢性肝病的常见并发症，失控的细胞增殖和过度沉积的胶原是其主要特征。长链非编码RNA ROR（lincRNA-ROR）在多种疾病中扮演着重要角色。本研究对lincRNA-ROR在肝纤维化中的作用机制进行了深入的探究。实验结果表明，lincRNA-ROR的表达水平在肝纤维化病变组织中显著升高。通过建立肝纤维化模型，我们发现lincRNA-ROR通过miR-145/ZEB2调控HERC5介导的p53蛋白ISG化修饰在肝纤维化中发挥了重要作用。这为肝纤维化的治疗提供了新的分子靶点和治疗策略。
关键词：肝纤维化、lincRNA-ROR、miR-145/ZEB2、HERC5、p53蛋白ISG化修饰
Abstract:
Hepatic fibrosis is a common complication of chronic liver dia, and uncontrolled cell proliferation and excessive deposition of collagen are its main characteristics. Long non-co
用法的英文ding RNA ROR (lincRNA-ROR) plays an important role in various dias. In this study, we explored the mechanism of lincRNA-ROR in liver fibrosis. The results showed that the expression level of lincRNA-ROR was significantly incread in liver fibrosis tissues. By establishing a liver fibrosis model, we found that lincRNA-ROR mediated by miR-145/ZEB2 regulates HERC5-mediated p53 protein ISG modification plays an important role in liver fibrosis. This provides a new molecular target and treatment strategy for the treatment of liver fibrosis.
江晚正愁余Keywords: liver fibrosis, lincRNA-ROR, miR-145/ZEB2, HERC5, p53 protein ISG modification
公务员考什么科目Liver fibrosis is a complex dia that can result in the development of cirrhosis and liver cancer. It is characterized by the accumulation of excess collagen and other extracellular matrix components in the liver. This process is associated with the activation of hepatic stellate cells (HSCs) and the cretion of pro-inflammatory cytokines and growth factors. Despite extensive rearch, the molecular mechanisms driving liver fibrosis remain poorly understood.
In recent years, long noncoding RNAs (lncRNAs) have emerged as important regulators of gene expression in many biological process, including fibrosis. LincRNA-ROR is a well-known lncRNA that has been implicated in cancer, stem cell pluripotency, and neuronal differentiation. However, its role in liver fibrosis is not yet clear. 如何学习数学
In this study, we investigated the expression and function of lincRNA-ROR in liver fibrosis. We found that the expression level of lincRNA-ROR was significantly incread in liver fibrosis tissues compared to healthy controls. We then established a liver fibrosis model in mice and found that lincRNA-ROR played a critical role in the development and progression of liver fibrosis.
Further analysis revealed that lincRNA-ROR regulated a key pathway involved in liver fibrosis. Specifically, lincRNA-ROR mediated the interaction between miR-145 and ZEB2, which is a transcription factor that promotes HSC activation and fibrosis. By modulating this pathway, lincRNA-ROR was able to regulate the expression of HERC5, which is involved in the modification of the p53 protein by interferon-stimulated genes (ISGs). This 木瓜怎么煲汤
modification is important for the activation of p53 and the induction of apoptosis in activated HSCs, which can slow or rever the progression of liver fibrosis.
Our findings suggest that lincRNA-ROR may be a promising molecular target for the treatment of liver fibrosis. By modulating its expression or activity, it may be possible to slow or even rever the progression of this dia. Further studies are needed to confirm the findings in human patients and to develop effective therapeutic strategies
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In addition to lincRNA-ROR, other potential molecular targets have been identified for the treatment of liver fibrosis. One such target is miR-29, which has been shown to inhibit collagen synthesis and reduce the verity of liver fibrosis in animal models. Another target is galectin-3, a carbohydrate-binding protein that plays a role in fibrosis by promoting the activation of HSCs. Inhibition of galectin-3 has been shown to reduce liver fibrosis in animal models.
In addition to targeting specific molecules, there are also approaches that focus on modulating the immune respon to liver injury. For example, drugs that inhibit TGF-β sig
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naling have been shown to reduce liver fibrosis by blocking the activation of HSCs and promoting the activity of immune cells that help to resolve fibrosis. Similarly, modulation of the gut microbiome has been shown to have a potential therapeutic effect on liver fibrosis, as the gut microbiome has been shown to play a role in the development and progression of this dia.
While there are a number of potential molecular targets and therapeutic strategies for the treatment of liver fibrosis, there is still much to be learned about this dia. Further studies are needed to fully understand the molecular mechanisms that drive liver fibrosis and to identify new therapeutic targets. Additionally, clinical studies are needed to test the safety and efficacy of novel therapies in human patients. With continued rearch and development, it is hoped that effective treatments for liver fibrosis will become available to patients in the near future
