Related Experiment Video

Updated: Aug 11, 2026

En Face Detection of Nitric Oxide and Superoxide in Endothelial Layer of Intact Arteries
08:58

En Face Detection of Nitric Oxide and Superoxide in Endothelial Layer of Intact Arteries

Published on: February 25, 2016

Involvement of the nicotinamide adenosine dinucleotide phosphate oxidase isoform Nox2 in cardiac contractile

David J Grieve1, Jonathan A Byrne, Anjana Siva

  • 1King's College London, Cardiovascular Division, Guy's, King's, and St. Thomas' School of Medicine, London, England.

Journal of the American College of Cardiology
|February 21, 2006
PubMed
Abstract

Insights

The Nox2 enzyme contributes to heart dysfunction and fibrosis in pressure-overload left ventricular hypertrophy (LVH) but is not essential for the condition's development. Its inhibition preserves cardiac function during LVH.

Area of Science:

  • Cardiovascular Research
  • Molecular Biology
  • Physiology

Background:

  • Reactive oxygen species (ROS) are key in left ventricular hypertrophy (LVH) pathophysiology.
  • Nox2, a ROS-producing enzyme, is involved in angiotensin II-induced hypertrophy but not essential for pressure-overload LVH.
  • The specific role of Nox2 in contractile dysfunction during pressure-overload LVH remains unclear.

Purpose of the Study:

  • To investigate the role of Nox2 in contractile dysfunction in pressure-overload induced left ventricular hypertrophy (LVH).
  • To determine if Nox2 inhibition can mitigate cardiac dysfunction and fibrosis associated with LVH.

Main Methods:

  • Comparison of cardiac contractile function and interstitial fibrosis in Nox2 knockout (Nox2-/-) and wild-type (WT) mice subjected to aortic banding or sham surgery.
  • Echocardiography and pressure-volume analyses were used to assess left ventricular (LV) function.
  • Assessment of interstitial fibrosis and procollagen mRNA expression.

Main Results:

  • Aortic banding induced similar increases in LV mass in both Nox2-/- and WT mice.
  • Banded Nox2-/- mice exhibited significantly better LV function and preserved contractility compared to banded WT mice.
  • Interstitial fibrosis and procollagen expression were elevated in banded WT mice but not in Nox2-/- mice, suggesting Nox2's role in fibrosis development.

Conclusions:

  • Nox2 oxidase plays a significant role in cardiac contractile dysfunction and interstitial fibrosis during pressure overload.
  • Nox2 is not essential for the development of morphologic hypertrophy itself.
  • These findings indicate distinct downstream effects of Nox2 on different aspects of the pressure overload response.

More Related Videos

Contractility Measurements on Isolated Papillary Muscles for the Investigation of Cardiac Inotropy in Mice06:22

Contractility Measurements on Isolated Papillary Muscles for the Investigation of Cardiac Inotropy in Mice

Published on: September 17, 2015

Cardiac Catheterization in Mice to Measure the Pressure Volume Relationship: Investigating the Bowditch Effect07:38

Cardiac Catheterization in Mice to Measure the Pressure Volume Relationship: Investigating the Bowditch Effect

Published on: June 14, 2015

Related Concept Videos

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...
Pathophysiology of Cardiac Performance01:29

Pathophysiology of Cardiac Performance

Typical heart performance is influenced by heart rate, rhythm, myocardial contraction, and metabolism or blood flow. The cardiac muscle exhibits distinct electrophysiological features, including pacemaker activity and calcium channel control, which play a vital role in the heart's response to various drugs. The autonomic nervous system, comprising the sympathetic and parasympathetic branches, regulates heart rate. Sympathetic activation increases heart rate, while parasympathetic activation...
Heart Failure II: Pathophysiology01:29

Heart Failure II: Pathophysiology

Systolic Heart Failure and Compensatory MechanismsSystolic heart failure (also termed HFrEF, Heart Failure with Reduced Ejection Fraction) is the most prevalent type of heart filure. It results in a decreased volume of blood being pumped from the ventricle. The aortic arch and carotid sinuses have baroreceptors that detect reduced blood pressure, triggering the sympathetic nervous system (SNS) to release epinephrine and norepinephrine. Initially, this response aims to boost heart rate and...
Pathophysiology of Heart Failure01:17

Pathophysiology of Heart Failure

Heart failure (HF) is a progressive syndrome involving ventricles that leads to inadequate cardiac output. It can be classified based on location and output or ejection fraction. Ejection fraction (EF) is an essential measurement in the diagnosis and surveillance of HF. Reduced EF corresponds to systolic heart failure (HFrEF). However, HF with preserved ejection fraction (HFpEF) is becoming increasingly prevalent. Also known as diastolic HF, this form of HF is related to aging. The...
Electron Transport Chain: Complex III and IV01:43

Electron Transport Chain: Complex III and IV

During the electron transport chain, electrons from NADH and FADH2 are first transferred to complexes I and II, respectively. These two complexes then transfer the electrons to ubiquinol, which carries them further to complex III. Complex III passes the electrons across the intermembrane space to Cyt c, which carries them further to complex IV. Complex IV donates electrons to oxygen and reduces it to water. As electrons pass through complexes I, III, and IV, the energy released aids the pumping...