在糖尿病病中,MiR-183-5p通过向TTP来调节炎症反应和亡
1Department of Geriatric Medicine, Nantong First People's Hospital Nantong 226000, Jiangsu, China.
American journal of translational research
|January 19, 2026
概括
微RNA-183-5p通过向tristetraprolin (TTP) 加快糖尿病病 (DN),增加炎症和亡. 抑制miR-183-5p为DN提供了一个潜在的治疗策略.
科学领域:
- 分子生物学分子生物学
- 内分泌学 在内分泌学.
- 腎臟病學 (nephrology) 是一種醫學專業.
背景情况:
- 糖尿病病 (DN) 是糖尿病的一个主要并发症.
- 微RNA及其点在DN病原体中的作用尚未完全理解.
研究的目的:
- 调查miR-183-5p和tristetraprolin (TTP) 在糖尿病病 (DN) 中的作用.
- 探索miR-183-5p,TTP和DNA中的炎症性细胞因子之间的关系.
主要方法:
- 对30名参与者进行了回顾性研究 (10名DN,10名T2DM,10名对照).
- 检测miR-183-5p和TTP表达水平.
- 分析miR-183-5p,TTP和炎症性细胞因子之间的相关性.
- 使用HK-2细胞进行体外研究,通过qRT-PCR和ELISA评估TTP和细胞因子表达.
主要成果:
- 在高血糖的情况下,miR-183-5p促进炎症和亡.
- TTP是miR-183-5p的一个直接目标.
- 升高的miR-183-5p增加了HK-2细胞中的炎症性细胞因子释放和亡.
- miR-183-5p抑制剂降低了炎症性细胞因子水平.
结论:
- miR-183-5p通过准TTP来加速DN的发展.
- 这种相互作用为DN治疗提供了一个新的治疗点.
相关概念视频
07:15Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway
872
The present protocol describes the establishment of a membranous nephropathy (MN) animal model, and how Kemeng Fang's inhibition reduces MN rat podocyte apoptosis by activating the PI3K/AKT signaling...
872
08:15Antagonistic Effect of Jiawei Shengjiang San on a Rat Model of Diabetic Nephropathy: Related to EGFR/MAPK3/1 Signaling Pathway
924
Here, we present a protocol describing network pharmacology and molecular docking techniques to explore the mechanism of action of Jiawei Shengjiang San (JWSJS) in treating diabetic...
924
07:45Tear-Derived Exosomal miR-15a as New Diagnostic Tool for Diabetic Retinopathy
276
This article describes a protocol for the collection and detection of miR-15a from tears as a new diagnostic tool for diabetic...
276
Inflammatory Response
16.1K
An inflammatory response is a localized, nonspecific immune reaction that occurs when a tissue is injured. It is characterized by redness, swelling, heat, and pain, which are commonly called the cardinal signs and symptoms of inflammation. Inflammation can sometimes result in a loss of function.
Inflammation can be triggered by various stimuli, such as impact, abrasion, chemical irritation, infections, and extreme hot or cold temperatures. These can damage cells and connective tissue fibers,...
Inflammation can be triggered by various stimuli, such as impact, abrasion, chemical irritation, infections, and extreme hot or cold temperatures. These can damage cells and connective tissue fibers,...
16.1K
Inflammatory Response II: Inflammatory Exudate and Tissue Repair
7.5K
The immune system's inflammatory response destroys the invading pathogen, permitting the tissue to heal. The changes during the cellular and vascular stages allow exudate formation at the site of inflammation. The inflammatory exudate released from the wound has high protein content and a specific gravity above 1.020.
The typical wound exudate is odorless, transparent, straw-colored, thin, and watery. Exudate, however, can differ depending on the state of wound healing. Likewise, the...
The typical wound exudate is odorless, transparent, straw-colored, thin, and watery. Exudate, however, can differ depending on the state of wound healing. Likewise, the...
7.5K
Inflammatory Response I: Vascular and Cellular
16.1K
The inflammatory response is the body's defense against infection, injury, or irritation from bacteria, trauma, toxins, or heat. Inflammation helps locate and destroy pathogens and remove damaged tissue elements to heal the body. During this initial phase, fluid, blood products, and nutrients migrate to the injured area, resulting in redness, heat, swelling, ache, and loss of function. Moreover, signs of systemic inflammation include fever, increased WBC count, malaise, anorexia, nausea,...
16.1K


