相关实验视频

Updated: Jun 3, 2025

Experimental Model of Ligature-Induced Peri-Implantitis in Mice

Experimental Model of Ligature-Induced Peri-Implantitis in Mice

Published on: May 17, 2024

细胞类型特定的ROS-AKT/mTOR-自相互作用 - - 在周植入炎中应解决吗?

Mihai Butucescu¹, Marina Imre², Florentina Rus-Hrincu³

¹Department of Organization, Professional Legislation and Management of the Dental Office, Faculty of Dental Medicine, "Carol Davila" University of Medicine and Pharmacy, 17-23 Plevnei Street, 020021 Bucharest, Romania.

Diagnostics (Basel, Switzerland)

|January 8, 2025

概括

周植入炎是一种导致植入失败的炎症性疾病,涉及复杂的相互作用. 了解AKT/mTOR信号传递,自和反应性氧物种 (ROS) 之间的相互作用是预防周植入炎的关键.

科学领域:

口腔生物学和病理学
生物医学工程生物医学工程
炎症性疾病研究的研究.

背景情况:

周植入体炎是导致牙植入物失败的主要原因,其特点是炎症和骨质损失.
自和AKT/mTOR通路是炎症反应的关键调节者.
周植入炎中这些通路之间的复杂交叉并未完全理解.

研究的目的:

审查当前关于反应性氧物种 (ROS) 在AKT/mTOR信号传递和在周植入炎中的自相互作用中的作用的数据.
探索这些相互作用的关键细胞类型涉及到围植入炎的发病.
突出了解这些细胞机制的临床意义.

主要方法:

对现有研究的文献综述周植入炎,AKT/mTOR信号传递,自和ROS.
分析这些途径在涉及周植入炎的不同细胞类型中的参与.
综合数据以确定治疗目标和临床影响.

主要成果:

反应性氧物种 (ROS) 显著影响了AKT/mTOR信号传递和周植入炎中自之间的相互作用.
涉及这些途径的特定细胞机制有助于植入周炎的发展和进展.
在不同细胞类型中调节自可能提供治疗策略.

结论:

通过ROS调节的AKT/mTOR-自轴的向,为周植入炎的预防和治疗提供了一个有希望的途径.
细胞特异性的自细胞调节可以帮助优化骨质整合并防止植入物失败.
对这些复杂的细胞相互作用的进一步研究对于植入式牙科的临床进展至关重要.

关键词:

这就是ROSOS ROS.自自是自的过程.自调节器是自调节器.树突细胞是一种树突细胞.牙纤维细胞牙纤维细胞巨细胞是什么?巨细胞是什么?骨质母细胞 (osteoblasts) 是一个骨质细胞.这些骨质细胞是骨质细胞.周植入体炎 (periimplantitis) 是一种发生在周植入体周边的疾病.

更多相关视频

Inducing Apical Periodontitis in Mice

Inducing Apical Periodontitis in Mice

Published on: August 6, 2019

Robust Ligature-Induced Model of Murine Periodontitis for the Evaluation of Oral Neutrophils

Robust Ligature-Induced Model of Murine Periodontitis for the Evaluation of Oral Neutrophils

Published on: January 21, 2020

相关概念视频

PI3K/mTOR/AKT Signaling Pathway

PI3K/mTOR/AKT Signaling Pathway

The mammalian target of rapamycin (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1 (mTORC1) and mTOR complex 2 (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast, mTORC2 consists of a...

mTOR Signaling and Cancer Progression

mTOR Signaling and Cancer Progression

The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
The mTOR pathway or the...

The JAK-STAT Signaling Pathway

The JAK-STAT Signaling Pathway

Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as SH2...

Autophagy

Autophagy

Autophagy is a self-digesting process by which a cell protects itself from threats both within and outside the cell, ranging from abnormal proteins to invading bacteria. In this process, obsolete components of the cell and invading microbes are degraded by hydrolytic enzymes active in an acidic environment of the lysosomal lumen.
An autophagic pathway consists of a series of signaling events activated in response to diverse stress and physiological conditions such as food deprivation,...