Jove
Visualize
お問い合わせ
JoVE
x logofacebook logolinkedin logoyoutube logo
JoVEについて
概要リーダーシップブログJoVEヘルプセンター
著者向け
出版プロセス編集委員会範囲と方針査読よくある質問投稿
図書館員向け
推薦の声購読アクセスリソース図書館諮問委員会よくある質問
研究
JoVE JournalMethods CollectionsJoVE Encyclopedia of Experimentsアーカイブ
教育
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab Manual教員リソースセンター教員サイト
利用規約
プライバシーポリシー
ポリシー

関連する概念動画

Cholesterol: Significance and Regulation01:29

Cholesterol: Significance and Regulation

1.7K
Although not a source of energy, cholesterol plays a significant role as a foundational structure for bile salts, steroid hormones, and vitamin D, as well as being a crucial component of plasma membranes. Approximately 15% of blood cholesterol is derived from our diet, with the remainder synthesized from acetyl CoA by the liver and intestines. Cholesterol is eliminated from the body through its conversion into bile salts, which are eventually discarded in the feces.
Considering cholesterol and...
1.7K
Atherosclerosis III: Management01:26

Atherosclerosis III: Management

482
Management of atherosclerosis involves an integrated strategy encompassing pharmacological treatment, surgical interventions, lifestyle changes, and nutrition therapy to address the multifactorial nature of the disease.Pharmacological TherapyA cornerstone of atherosclerosis management is the use of pharmacological agents. Statins, such as atorvastatin, are pivotal in inhibiting HMG-CoA reductase, an enzyme that catalyzes an initial step in cholesterol synthesis in the liver. This reduction in...
482
Atherosclerosis I: Introduction01:30

Atherosclerosis I: Introduction

1.5K
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...
1.5K
Regulation of Nuclear Protein Sorting01:45

Regulation of Nuclear Protein Sorting

3.4K
Nuclear protein sorting regulates nucleus composition and gene expression, crucial for determining the fate of a eukaryotic cell. Hence, the entry and exit of molecules across the nuclear envelope is a tightly controlled process. Nuclear protein sorting can be inhibited by one of the following ways: 1) masking cargo signal sequences, 2) modifying the nuclear receptor's affinity for cargo, 3) controlling the nuclear pore size, 4) retaining the cargo during its transit to the cytosol or the...
3.4K
Lipid-Lowering Drugs: Statins and Miscellaneous Agents01:20

Lipid-Lowering Drugs: Statins and Miscellaneous Agents

1.6K
Hyperlipidemia, a medical condition often referred to as high cholesterol, is characterized by abnormally elevated levels of lipids in the bloodstream. When present in excess, these lipids, specifically cholesterol and triglycerides, can lead to serious health complications, often involving cardiovascular diseases. Illnesses like atherosclerosis, heart attacks, and pancreatitis have all been linked to untreated hyperlipidemia. This means controlling and regulating cholesterol and triglyceride...
1.6K
Transducer Mechanism: Nuclear Receptors01:31

Transducer Mechanism: Nuclear Receptors

3.3K
Nuclear receptors, or NRs, are unique transcription factors that regulate gene transcription and affect the cellular pathways involved in reproduction, development, or metabolism. Their ability to be stimulated by small lipophilic ligands and control vital cellular processes makes them ideal drug targets. Nearly 10-15% of currently prescribed drugs target these receptors.
About 48 different soluble family members of nuclear receptors are identified that can be divided into two main classes:
3.3K
このページは機械翻訳されています。他のページは英語で表示される場合があります。View in English
  1. ホーム
  3. 研究分野
  5. 生物医学と臨床科学
  7. 心血管医学と血液学
  9. 心臓病 (心血管疾患を含む)
  11. クリュッペルのような因子4 コレステロール25ヒドロキシラーゼと肝臓x受容体の調節 動脈硬化症の感受性を軽減する

クリュッペルのような因子4 コレステロール25ヒドロキシラーゼと肝臓X受容体の調節 動脈硬化症の感受性を軽減する

Zhao Li1, Marcy Martin1, Jin Zhang1

  • 1From Cardiovascular Research Center, School of Basic Medical Sciences, Xi'an Jiaotong University Health Science Center, China (Z.L., Jin Zhang, L.B., Jiao Zhang, M.H., J.L., T.L., J.Y.-J.S.); Key Laboratory of Environment and Genes Related to Diseases, Xi'an Jiaotong University, Ministry of Education of China (Z.L., Jin Zhang, L.B., Jiao Zhang, M.H., J.L., T.L., J.Y.-J.S.); Division of Cardiology, Department of Medicine, University of California, San Diego, La Jolla (M.M., Jin Zhang, J.K., M.H., Y.-J.X., M.J., J.Y.-J.S.);Department of Bioengineering, University of California, San Diego, La Jolla (M.R.M., S.G.); Division of Biochemistry and Molecular Biology, University of California, Riverside (M.M.); Institute of Bioinformatics and Systems Biology and Department of Biological Science and Technology, National Chiao Tung University, Hsin-Chu, Taiwan (H.-Y.H., H.-D.H.); and Department of Medicine, Case Western Reserve University School of Medicine, Cleveland, OH (G.Z., P.S., M.K.J.).

Circulation
|August 11, 2017

関連する実験動画

Quantification of Atherosclerosis in Mice
06:59

Quantification of Atherosclerosis in Mice

Published on: June 12, 2019

40.6K
LDL Cholesterol Uptake Assay Using Live Cell Imaging Analysis with Cell Health Monitoring
08:45

LDL Cholesterol Uptake Assay Using Live Cell Imaging Analysis with Cell Health Monitoring

Published on: November 17, 2018

14.2K
Quantitative Determination of De Novo Fatty Acid Synthesis in Brown Adipose Tissue Using Deuterium Oxide
07:34

Quantitative Determination of De Novo Fatty Acid Synthesis in Brown Adipose Tissue Using Deuterium Oxide

Published on: May 12, 2023

1.6K

PubMed で要約を見る

まとめ
この要約は機械生成です。

クリュッペルのような因子4 (KLF4) は,コレステロール25ヒドロキシラーゼ (Ch25h) と肝臓X受容体 (LXR) を活性化し,炎症を抑制し,動脈硬化から保護します. このKLF4-Ch25h/LXR軸は,内皮細胞とマクロファージの間の相乗効果を促進する.

キーワード:
動脈硬化症コレステロール内皮細胞炎症

関連する実験動画

Quantification of Atherosclerosis in Mice
06:59

Quantification of Atherosclerosis in Mice

Published on: June 12, 2019

40.6K
LDL Cholesterol Uptake Assay Using Live Cell Imaging Analysis with Cell Health Monitoring
08:45

LDL Cholesterol Uptake Assay Using Live Cell Imaging Analysis with Cell Health Monitoring

Published on: November 17, 2018

14.2K
Quantitative Determination of De Novo Fatty Acid Synthesis in Brown Adipose Tissue Using Deuterium Oxide
07:34

Quantitative Determination of De Novo Fatty Acid Synthesis in Brown Adipose Tissue Using Deuterium Oxide

Published on: May 12, 2023

1.6K

科学分野:

  • 心血管生物学
  • 免疫学
  • 分子生物学

背景:

  • 動脈硬化症は,内皮細胞 (ECs) と単細胞/マクロファージなどの免疫細胞を含む複雑な炎症性疾患である.
  • コレステロール25ヒドロキシコレステロール (Ch25h) によって調節される25ヒドロキシコレステロールは,肝臓X受容体 (LXR) リガンドおよびステロール調節因子結合タンパク質2 (SREBP2) 阻害体として作用することで,細胞の炎症およびコレステロール代謝に影響します.

研究 の 目的:

  • コレステロール酸化と流出遺伝子の制御における クリュッペル型因子4 (KLF4) の役割を調査する.
  • 内皮細胞とマクロファージにおけるKLF4-Ch25h/LXR経路の動脈保護機能を調査する.

主な方法:

  • KLF4調節遺伝子を特定するためにRNA配列データをバイオ情報分析.
  • 培養されたECとマクロファージを用いたin vitro試験
  • Ch25hを消去したマウスを使った体内実験.

主要な成果:

  • 血管保護刺激により,KLF4経由で Ch25hとLXRの発現が上昇した.
  • KLF4- Ch25h/ LXR軸は,ECの炎症体活性を低下させ,M1からM2のマクロファージの偏化を促進することによって,炎症を抑制した.
  • アポリポプロテイン E-/ Ch25h-/ マウスでは動脈硬化が悪化し,軸の保護的役割が確認された.

結論:

  • KLF4はCh25hとLXRの表現を直接トランザクティブにする.
  • この活性化により,ECとマクロファージの間の保護的な相乗効果が促進され,動脈硬化症の感受性を軽減します.
マクロファージ
切断ストレス