相关实验视频

Updated: Jun 23, 2025

Incorporation of a Survivable Liver Biopsy Procedure in Mice to Assess Non-alcoholic Steatohepatitis NASH Resolution

Incorporation of a Survivable Liver Biopsy Procedure in Mice to Assess Non-alcoholic Steatohepatitis NASH Resolution

Published on: April 16, 2019

肠道NSD2通过质子修饰加剧非酒精性脂肪肝炎

Yijia Zhang^1,2, Yuan Qiao², Zecheng Li²

¹Beijing Key Laboratory of Bioprocess, College of Life Science and Technology, Beijing University of Chemical Technology, Beijing, 100029, P. R. China.

Advanced science (Weinheim, Baden-Wurttemberg, Germany)

|June 26, 2024

概括

这项研究确定了核受体结合SET域蛋白2 (NSD2) 作为非酒精性脂肪肝炎 (NASH) 进展的关键因素. 准肠道NSD2可能为治疗NASH提供新的治疗策略.

科学领域:

胃肠病学胃肠病学
分子生物学分子生物学
代谢疾病代谢疾病

背景情况:

受损的肠道屏障越来越多地与非酒精性脂肪肝炎 (NASH) 的进展有关.
在NASH中驱动这种肠道功能障碍的特定分子机制尚不清楚.

研究的目的:

研究核受体结合SET域蛋白2 (NSD2) 在与非酒精性脂肪肝炎 (NASH) 相关的肠壁功能障碍中的作用.
阐明NSD2影响肠道屏障完整性和NASH病变的分子机制.

主要方法:

从肥胖人类和高脂肪胆固醇饮食 (HFCD) 的小鼠的肠道组织中检查了NSD2表达.
利用小鼠的肠道特异性NSD2淘汰和过度表达模型来评估对肠道屏障功能和NASH的影响.
研究了NSD2的表观遗传调节,特别是其在素H3 lysine 36二甲基化 (H3K36me2) 中的作用及其对Ern1基因表达和ERN1-JNK信号通路的影响.

主要成果:

在肥胖人类和食HFCD的小鼠的肠道中发现了显著的NSD2上调.
肠道特异性NSD2淘汰赛减弱了肠道屏障损伤和NASH进展.
NSD2过度表达加剧了肠道屏障缺陷和NASH.
证明NSD2通过H3K36me2脱甲基化直接促进Ern1的转录激活,激活ERN1-JNK轴.

结论:

通过H3K36me2表观遗传修饰,NSD2在调解肠道屏障损伤方面发挥着至关重要的作用.
通过NSD2介导的ERN1-JNK通路的激活有助于NASH的进展.
准肠道NSD2为管理NASH提供了一个潜在的新疗法策略.

关键词:

肝脏肥胖症肝脏肥胖症基因组二甲基转移酶的基因组二甲基转移酶.肠道屏障肠道屏障肠道屏障紧密的交叉路口紧密的连接

更多相关视频

An Advanced Murine Model for Nonalcoholic Steatohepatitis in Association with Type 2 Diabetes

An Advanced Murine Model for Nonalcoholic Steatohepatitis in Association with Type 2 Diabetes

Published on: April 26, 2019

A Model of Experimental Steatosis In Vitro: Hepatocyte Cell Culture in Lipid Overload-Conditioned Medium

A Model of Experimental Steatosis In Vitro: Hepatocyte Cell Culture in Lipid Overload-Conditioned Medium

Published on: May 18, 2021

相关概念视频

Role Of Notch Signalling In Intestinal Stem Cell Renewal

Role Of Notch Signalling In Intestinal Stem Cell Renewal

Notch signaling was first discovered in Drosophila melanogaster, where it is involved in cell lineage differentiation. Notch signaling regulates the maintenance and differentiation of intestinal stem cells or ISCs by controlling the expression of atonal homolog 1 or Atoh1. Atoh1 directs cells to differentiate into secretory cells.
Direct cell-to-cell contact is needed for the activation of Notch signaling. The signal is initiated when a notch ligand binds to a receptor on an adjacent cell, also...

NF-κB-dependent Signaling Pathway

NF-κB-dependent Signaling Pathway

The transcription factor NF-κB was discovered in 1986 in the lab of Nobel laureate Professor David Baltimore, for its interaction with the immunoglobulin light chain enhancer in B-cells. After more than three decades of study, it is now evident that NF-κB regulates the expression of over 100 genes. Most of these genes play an essential role in the innate and adaptive immune responses as well as the inflammatory responses of animals.
NF-κB-dependent Signaling Mechanism
The...

Gastritis-II: Pathophysiology

Gastritis-II: Pathophysiology

Gastritis is marked by disruption of the mucosal barrier that usually protects the stomach tissue from digestive juices and manifests in acute and chronic forms.
In acute gastritis, the gastric mucosa becomes swollen and red and undergoes superficial erosion. Superficial ulceration may lead to bleeding.
In chronic gastritis, persistent or repeated insults lead to chronic inflammatory changes and, eventually, thinning or atrophy of the gastric tissue.
Gastritis can stem from various causes, each...