AGE (RAGE) の受容体は,動脈損傷に対する反応としてネオインティマル形成を媒介する
Zhongmin Zhou1, Kai Wang, Marc S Penn
1Experimental Interventional Laboratory, Department of Cardiovascular Medicine, The Cleveland Clinic Foundation, Cleveland, Ohio 44195, USA.
Circulation
|April 30, 2003
まとめ
アドバンスト・グリケーション・エンド・プロダクト (RAGE) 経路の受容体阻害により,血管損傷後のネオインティマル・ハイパープラジアが著しく減少しました. このRAGE/リガンドの相互作用は,糖尿病に関係なく,ネオインティマルの形成の重要な要因です.
科学分野:
- 血管生物学 血管生物学
- セルラー・シグナリング
- 糖尿病による合併症
背景:
- アドバンスト・グリケーション・エンド・プロダクト (RAGE) の受容体とそのリガンド (AGEs,S100/カルグランウリン) は,様々な疾患に関与しています.
- 血管損傷後のネオインティマル・ハイパープラジアにおけるRAGE/リガンド相互作用の特定の役割は十分に理解されていません.
研究 の 目的:
- 血管損傷後のネオインティマル・ハイパープラジアにおけるRAGE/リガンド相互作用の役割を調査する.
- RAGE/リガンドの相互作用を阻害する治療の可能性を評価する.
主な方法:
- 糖尿病と非糖尿病のラットで気球損傷後のRAGEとリガンド発現を調べた.
- RAGEとリガンドの相互作用を阻害するために,溶性RAGEを使用しました.
- 評価された血管滑らかな筋肉細胞 (VSMC) 増殖 in vitro および in vivo.
- 定量化されたネオインティマルの形成と光の領域の変化.
主要な成果:
- 糖尿病のネズミは,非糖尿病のネズミと比較して,AGEの蓄積とRAGE/S100の免疫反応の増加を示した.
- RAGE/リガンドの相互作用を阻害することで,S100刺激によるVSMCの増殖を in vitroで減少させました.
- In vivoでは,RAGE阻害は,増殖するVSMCを減少させ,ネオインティマルの形成を抑制し,糖尿病と非糖尿病の両方のラットで光面面積を増加させた.
結論:
- RAGE/リガンドの相互作用は,糖尿病状態とは関係なく,血管損傷後のネオインティマルの形成に不可欠です.
- RAGE/リガンドの相互作用をターゲットにすることで,ネオインティマール・ハイパープラジアを緩和するための新しい治療戦略が提示されます.
さらに関連する動画
08:41Assessment of Vascular Tone Responsiveness using Isolated Mesenteric Arteries with a Focus on Modulation by Perivascular Adipose Tissues
Published on: June 3, 2019
9.5K
05:41Using a Cell-Tracer Injection to Investigate the Origin of Neointima-Forming Cells in a Rat Saccular Side Wall Model
Published on: March 16, 2022
1.7K
関連する概念動画
01:38Inflammation
46.8K
Overview
46.8K
01:10Mechanism of Angiogenesis
6.4K
Blood vessel formation starts early during embryonic development, around day 7. In the extraembryonic yolk sac, mesodermal precursor cells called hemangioblast proliferate and differentiate into angioblast. Angioblasts express vascular endothelial growth factor receptor 2 or VEGFR2, which binds VEGF-A, a proangiogenic factor, guiding blood vessel formation. VEGF signaling promotes angioblasts to form a blood island in the developing embryo. Angioblasts further differentiate, giving rise to...
6.4K
01:24Regulation of Angiogenesis and Blood Supply
2.9K
Rapidly dividing tumors, embryos, and wounded tissues require more oxygen than usual, lowering the oxygen concentration in the blood. At low oxygen or hypoxic conditions, an oxygen-sensitive transcription factor called the hypoxia-inducible factor 1 or HIF1 is activated. HIF1 is a dimeric protein of alpha (ɑ) and beta (β) subunits. Under optimal oxygen conditions, HIF1β is present in the nucleus while HIF1ɑ remains in the cytosol. HIF1ɑ is hydroxylated by prolyl...
2.9K
01:28Inflammatory Response
12.5K
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,...
12.5K
01:30Atherosclerosis I: Introduction
2.5K
Atherosclerosis is a progressive disorder characterized by the buildup of plaques on the arterial inner wall, causing them to narrow and harden over time. These plaques comprise lipids, calcium, blood components, carbohydrates, and fibrous tissue. The process primarily affects the intima of large and medium-sized arteries, reducing blood flow in any artery.Etiology and risk factorsThe cause of atherosclerosis is multifactorial, involving a complex interplay among endothelial injury, lipid...
2.5K
01:26Acute Inflammation I: Inflammatory Response
118
Acute inflammation is a rapid, short-lived physiological response to tissue injury or infection, designed to eliminate harmful agents and initiate repair. This tightly regulated process typically lasts from minutes to several days and is triggered by factors such as microbial invasion, physical trauma, or chemical injury.Recognition and Mediator ReleaseThe inflammatory response begins when resident immune cells—such as mast cells, macrophages, and dendritic cells—detect...
118