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Coronary Artery Disease II: Pathophysiology

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Radical Autoxidation

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Updated: Jun 4, 2026

Analysis of Oxidative Stress in Zebrafish Embryos
11:05

Analysis of Oxidative Stress in Zebrafish Embryos

Published on: July 7, 2014

[Oxidative stress and endothelial dysfunction].

C Urso1, G Caimi

  • 1Dipartimento di Medicina Interna, Malattie Cardiovascolari e Nefrourologiche, Università degli Studi di Palermo, Italia. caimigre@unipa.it

Minerva Medica
|February 15, 2011
PubMed
Summary
This summary is machine-generated.

Oxidative stress, driven by excess reactive oxygen species (ROS), damages blood vessels and impairs endothelial function. This imbalance contributes to major diseases like hypertension and cardiovascular disease.

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Imaging Approaches to Assessments of Toxicological Oxidative Stress Using Genetically-encoded Fluorogenic Sensors
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Last Updated: Jun 4, 2026

Analysis of Oxidative Stress in Zebrafish Embryos
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Imaging Approaches to Assessments of Toxicological Oxidative Stress Using Genetically-encoded Fluorogenic Sensors
09:33

Imaging Approaches to Assessments of Toxicological Oxidative Stress Using Genetically-encoded Fluorogenic Sensors

Published on: February 7, 2018

Area of Science:

  • Vascular Biology
  • Pathophysiology

Context:

  • Endothelial dysfunction and oxidative stress are central to numerous diseases, including hypertension, atherosclerosis, dyslipidemia, diabetes mellitus, cardiovascular disease, renal failure, and ischemia-reperfusion injury.
  • Reactive oxygen species (ROS) play a dual role, modulating cellular functions physiologically but causing endothelial damage in excess.

Purpose:

  • To elucidate the role of oxidative stress and reactive oxygen species (ROS) in endothelial dysfunction and associated diseases.
  • To highlight the NADPH-oxidase as a primary ROS source and its activation pathways.
  • To explain how ROS disrupt vascular tone and nitric oxide availability.

Summary:

  • Excessive ROS production, primarily from NADPH-oxidase, overwhelms antioxidant systems, leading to oxidative stress.
  • This oxidative stress induces endothelial damage via inflammation, apoptosis, and altered extracellular matrix.
  • ROS decrease nitric oxide availability, impairing endothelium-dependent vasodilation, a hallmark of many vascular diseases.

Impact:

  • Understanding these mechanisms is crucial for developing therapeutic strategies targeting oxidative stress in cardiovascular and other related diseases.
  • Identifies NADPH-oxidase activation by angiotensin II, shear stress, and hyperglycemia as key targets.
  • Provides insight into the altered vascular tone observed in various pathological conditions.