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相关概念视频

GPCR Desensitization01:12

GPCR Desensitization

G protein-coupled receptor (GPCR) signaling plays a crucial role in cell functioning. GPCR desensitization is an equally essential process. It allows cells to respond to changing environments and regain sensitivity to new stimuli while preventing unnecessary stimulation when no longer needed. Prolonged exposure to stimuli leads to GPCR desensitization. It involves blocking the receptors from binding and activating additional G proteins. This inhibits activation of downstream effectors, thereby...
GPCRs Regulate Adenylyl Cylase Activity01:09

GPCRs Regulate Adenylyl Cylase Activity

Some GPCRs transmit signals through adenylyl cyclase (AC), a transmembrane enzyme. AC helps synthesize second messenger cyclic adenosine monophosphate (cAMP). AC catalyzes cyclization reaction and converts ATP to cAMP by releasing a pyrophosphate. The pyrophosphate is further hydrolyzed to phosphate by the enzyme pyrophosphatase, which drives cAMP synthesis to completion. However, cAMP is rapidly degraded to 5′ AMP by the enzymes phosphodiesterase (PDE), preventing overstimulation of cells.
Two...
Nitric Oxide Signaling Pathway01:28

Nitric Oxide Signaling Pathway

Nitric oxide (NO), an inorganic gas, acts as a potent second messenger in most animal and plant tissues. NO diffuses out of the cells that produce it and enters the neighboring cells to generate a downstream response. NO synthase (NOS) catalyzes NO production by the deamination of the amino acid arginine. There are three isoforms of NOS. Endothelial cells have endothelial NOS (eNOS), nerve and muscle cells have neuronal NOS (nNOS), and macrophages produce inducible NOS (iNOS) upon exposure to...
Cholesterol: Significance and Regulation01:29

Cholesterol: Significance and Regulation

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...
Coronary Artery Disease II: Pathophysiology01:26

Coronary Artery Disease II: Pathophysiology

Coronary Artery Disease (CAD) originates from a series of events that impair the function of coronary arteries, the blood vessels responsible for delivering oxygen-rich blood to the heart muscle. The pathophysiology of CAD is closely linked to atherosclerosis, a chronic inflammatory and lipid-driven condition affecting the vascular endothelium.1. Endothelial DamageThe process begins with damage to the vascular endothelium, which serves as a protective barrier between the blood and the vessel...

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相关实验视频

Updated: Jun 16, 2026

Cholesterol Efflux Assay
07:54

Cholesterol Efflux Assay

Published on: March 6, 2012

高胆固醇血症对血管溶性瓜尼利基环酸酶的表达和功能的影响

Ute Laber1, Thorsten Kober, Verena Schmitz

  • 1Institut für Pharmakologie und Klinische Pharmakologie, Heinrich-Heine-Universität, Düsseldorf, Germany.

Circulation
|February 21, 2002
PubMed
概括

高胆固醇血症导致血管中功能障碍的可溶性瓜尼利基环酶 (sGC) 的过度表达. 这种情况是可逆的,可能会导致动脉样硬化发展.

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Last Updated: Jun 16, 2026

Cholesterol Efflux Assay
07:54

Cholesterol Efflux Assay

Published on: March 6, 2012

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

Enrichment of Mammalian Tissues and Xenopus Oocytes with Cholesterol
10:12

Enrichment of Mammalian Tissues and Xenopus Oocytes with Cholesterol

Published on: March 25, 2020

科学领域:

  • 心血管生物学 心血管生物学
  • 分子医学是分子医学.
  • 动脉样硬化研究 动脉样硬化研究

背景情况:

  • 内皮氧化 (NO) 介导的血管扩张依赖于可溶性瓜尼利基环酶 (sGC) 的激活.
  • 已知高胆固醇血症会在动物模型和人类中损害NO介导的血管扩张.

研究的目的:

  • 调查高胆固醇血症对可溶性瓜尼利环酶 (sGC) 的表达和功能的影响.

主要方法:

  • 子被养标准或富含胆固醇的饮食,持续时间不同.
  • 使用西班牙语的sGC子单位 (alpha1和beta1) 的大动脉表达量化.
  • 测量了对SNAP的血管放松和大动脉细胞溶中的sGC活性.

主要成果:

  • 高胆固醇血症导致子大动脉中sGC-alpha1和sGC-beta1亚单元的显著上调.
  • 尽管表达增加,但基底和NO刺激的sGC活性仅略有增强,血管扩张功效降低.
  • 过度表达的sGC局部化到亲密病变,在饮食正常化后,这些变化是可逆的.

结论:

  • 高胆固醇血症诱导了功能障碍的血管sGC的可逆过度表达.
  • 这种功能失调的sGC可能在动脉样硬化的发病过程中发挥作用.