Related Experiment Video
Updated: Jun 20, 2026
Angiogenesis in the Ischemic Rat Lung
Published on: February 8, 2013
Reactive oxygen species promote angiogenesis in the infarcted rat heart
Wenyuan Zhao1, Tieqiang Zhao, Yuanjian Chen
1Division of Cardiovascular Diseases, Department of Medicine, University of Tennessee Health Science Center, 956 Court Avenue, Memphis, TN 38163, USA.
Abstract:
The purpose of this study was to determine whether reactive oxygen species (ROS) promote cardiac angiogenesis following myocardial infarction (MI) and contribute to cardiac repair. Rats with MI were treated with or without antioxidants, tempol and apocynin. Hearts of these rats were collected at days 2, 4, 7 and 14 post-MI. We examined the spatial and temporal relationship between oxidative stress and angiogenesis as well as the potential regulation of ROS in cardiac angiogenesis. We found: (i) following MI, gp91(phox), a subunit of NADPH oxidase, a key enzyme for ROS production, was significantly increased in the border zone at day 2, followed by the infarcted myocardium at day 4, peaked at day 7 and declined at day 14, while superoxide dismutase was significantly reduced; (ii) malondialdehyde, a marker of oxidative stress, was significantly increased in the infarcted myocardium at day 7; (iii) pre-existing blood vessels in the infarcted myocardium underwent necrosis post-MI, whereas newly formed vessels appeared at the border zone at day 4, and then extended into the infarcted myocardium, where microvascular density peaked at day 7 and (iv) antioxidant treatment significantly reduced microvascular density in the infarcted myocardium at day 7. These observations suggest that following MI, angiogenesis is mostly active in the infarcted myocardium in the first week, which is temporally and spatially coincident with enhanced ROS. Suppression of angiogenesis by antioxidants indicates that ROS promote angiogenesis in the infarcted myocardium and contribute to cardiac repair. Further studies are required to determine the mechanisms responsible for ROS-mediated cardiac angiogenesis.
Insights
Reactive oxygen species (ROS) promote cardiac angiogenesis after myocardial infarction (MI), contributing to heart repair. Antioxidant treatment reduced this blood vessel formation, indicating ROS
Area of Science:
- Cardiovascular Research
- Regenerative Medicine
- Oxidative Stress Biology
Background:
- Myocardial infarction (MI) leads to significant cardiac damage and impaired repair.
- The role of reactive oxygen species (ROS) in post-MI cardiac repair, particularly angiogenesis, remains incompletely understood.
- Oxidative stress markers and angiogenic activity are key indicators of cardiac healing.
Purpose of the Study:
- To investigate if reactive oxygen species (ROS) promote cardiac angiogenesis following myocardial infarction (MI).
- To determine the contribution of ROS to cardiac repair mechanisms post-MI.
- To examine the spatial and temporal correlation between oxidative stress and angiogenesis in the infarcted heart.
Main Methods:
- Rats underwent myocardial infarction (MI) and were treated with or without antioxidants (tempol, apocynin).
- Cardiac tissues were collected at specific time points (days 2, 4, 7, 14) post-MI.
- Analysis included measurement of NADPH oxidase subunit (gp91(phox)), superoxide dismutase, malondialdehyde, and microvascular density.
Main Results:
- NADPH oxidase and malondialdehyde (oxidative stress markers) increased post-MI, peaking around day 7.
- Angiogenesis was observed in the infarcted myocardium, peaking at day 7, following initial blood vessel necrosis.
- Antioxidant treatment significantly reduced microvascular density, indicating ROS' role in promoting angiogenesis.
Conclusions:
- Reactive oxygen species (ROS) play a crucial role in promoting cardiac angiogenesis in the infarcted myocardium during the first week post-MI.
- ROS-mediated angiogenesis appears to be a significant contributor to cardiac repair following myocardial infarction.
- Further research is needed to elucidate the precise mechanisms of ROS-mediated cardiac angiogenesis.
Related Concept Videos
01:24Regulation of Angiogenesis and Blood Supply
01:10Mechanism of Angiogenesis