Jove
Visualize
Contact Us

Related Experiment Videos

Oxidant stress and endothelial cell dysfunction.

H Lum1, K A Roebuck

  • 1Department of Pharmacology, Rush Presbyterian St. Luke's Medical Center, 2242 W. Harrison St., Suite 260, Chicago, IL 60612, USA. hlum@rush.edu

American Journal of Physiology. Cell Physiology
|March 14, 2001
PubMed
Summary
This summary is machine-generated.

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Clinician and staff perspectives on potential disparities introduced by the rapid implementation of telehealth services during COVID-19: a mixed-methods analysis.

Translational behavioral medicine·2021
Same author

Dark CO<sub>2</sub>-fixation and diurnal malic acid fluctuations in the submerged-aquatic Isoetes storkii.

Oecologia·2017
Same author

Reactive oxygen species mediate high glucose-induced heparanase-1 production and heparan sulphate proteoglycan degradation in human and rat endothelial cells: a potential role in the pathogenesis of atherosclerosis.

Diabetologia·2011
Same author

6-Hydroxydopamine-induced alterations in blood-brain barrier permeability.

The European journal of neuroscience·2005
Same author

Osteolysis: basic science.

Clinical orthopaedics and related research·2002
Same author

The potential role of the osteoblast in the development of periprosthetic osteolysis: review of in vitro osteoblast responses to wear debris, corrosion products, and cytokines and growth factors.

The Journal of arthroplasty·2001
Same journal

Skeletal muscle biomass as an underappreciated fate of glucose.

American journal of physiology. Cell physiology·2026
Same journal

Proteomic profile of urinary extracellular vesicles from rats with lithium-induced nephrogenic diabetes insipidus.

American journal of physiology. Cell physiology·2026
Same journal

A non-hydrolyzable candesartan cilexetil analog reveals synergistic activation as a tractable mechanism for TMEM175 modulation.

American journal of physiology. Cell physiology·2026
Same journal

Mitochondrial Calcium Transport in Amino Acid Metabolism: From nutritional responses to metabolic regulation.

American journal of physiology. Cell physiology·2026
Same journal

N-linked glycosylation regulates SNAT2 trafficking and stability in pancreatic ductal adenocarcinoma cells.

American journal of physiology. Cell physiology·2026
Same journal

Oxaloacetate Inhibition of Succinate Dehydrogenase: Mechanism and Physiological Implications.

American journal of physiology. Cell physiology·2026
See all related articles
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Reactive oxygen species (ROS) signal cell changes, but high levels cause injury. This review details how ROS impairs endothelial barrier function and promotes leukocyte adhesion in vascular diseases.

Area of Science:

  • Cellular and Molecular Biology
  • Physiology
  • Pathophysiology

Background:

  • Reactive oxygen species (ROS) are crucial signaling molecules at low levels but cause cellular injury at high concentrations.
  • The vascular endothelium is a key target of oxidant stress, impacting vascular diseases.
  • Oxidant stress alters endothelial permeability and leukocyte adhesion via signal transduction pathways.

Purpose of the Study:

  • To review recent findings on the mechanisms of ROS signaling in endothelial dysfunction.
  • To elucidate how ROS impairs endothelial barrier function and promotes leukocyte adhesion.
  • To emphasize the regulation of adhesion molecules, cytoskeleton, and signal transduction.

Main Methods:

  • Literature review of recent findings on ROS and endothelial function.

Related Experiment Videos

  • Analysis of cellular and molecular mechanisms.
  • Focus on signal transduction pathways and redox-regulated transcription factors.

    • Main Results:

    • ROS signaling at higher concentrations leads to impaired endothelial barrier function.
    • Oxidant stress promotes leukocyte adhesion to the endothelium.
    • Alterations in cell-cell adhesion, cytoskeleton, and protein kinases are involved.

    Conclusions:

    • ROS play a dual role in cellular regulation, with detrimental effects at high concentrations on endothelial function.
    • Understanding ROS mechanisms is critical for addressing vascular diseases.
    • Further research on signal transduction and redox regulation is warranted.