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Updated: Jul 19, 2026
In Vitro Model of Coronary Angiogenesis
Published on: March 10, 2020
Transitional angiogenesis and vascular remodeling during coronary angiogenesis in response to myocardial infarction
Taren M Grass1, Diana I Lurie, J Douglas Coffin
1Center for Environmental Health Sciences, Department of Biomedical and Pharmaceutical Sciences, SB244, The University of Montana, Missoula, MT 59812, USA.
Insights
Coronary artery disease (CAD) triggers natural blood vessel growth (angiogenesis) after heart attacks. However, vascular remodeling limits long-term blood flow, suggesting therapies should target both processes for better heart perfusion.
Area of Science:
- Cardiovascular Science
- Regenerative Medicine
- Molecular Biology
Background:
- Coronary artery disease (CAD) is a leading cause of death, leading to myocardial ischemia and reduced quality of life.
- The heart naturally attempts to compensate for ischemia through angiogenesis, forming collateral circulation.
- Current research aims to enhance this natural process for therapeutic benefit.
Purpose of the Study:
- To characterize collateral circulation formation in a post-infarction mouse heart model.
- To define the morphogenic processes involved in collateral circulation development after myocardial infarction.
- To evaluate the impact of vascular remodeling on myocardial perfusion following therapeutic angiogenesis.
Main Methods:
- Utilized a transgenic mouse model with induced myocardial infarction via thoracotomy and microcauterization.
- Labeled coronary vessels to visualize and characterize neovascularization and collateral formation.
- Monitored angiogenesis and vascular remodeling at 1, 7, and 14 days post-treatment.
Main Results:
- The infarcted heart demonstrated consistent angiogenesis starting at 1 day post-treatment.
- Vascular remodeling was observed at 7 days, with complete remodeling by 14 days post-treatment.
- Vascular remodeling appeared to counteract early gains in myocardial perfusion from angiogenesis.
Conclusions:
- Therapeutic strategies for CAD should move beyond solely promoting angiogenesis.
- Modulating vascular remodeling is crucial for achieving sustained improvements in long-term myocardial perfusion.
- A dual approach targeting both angiogenesis and vascular remodeling may enhance treatment efficacy for coronary artery disease.
Abstract:
Coronary artery disease (CAD) is a major source of morbidity and mortality in the industrialized world. CAD causes ischemia as a prelude to angina, myocardial infarction and heart failure as specific forms of heart disease causing a decline in the quality of life. CAD or atherosclerosis and the resulting myocardial ischemia trigger a natural angiogenic response that generates collateral circulations. The long-term goal for these studies is to develop therapeutic angiogenesis that augments the natural coronary angiogenesis. This project makes use of an infarcted transgenic mouse model to characterize formation of those collateral circulations in the post-infraction heart. The experiments utilized thoracotomy and a microcauterizer to produce an infarct in transgenic mice and this stimulated neovascularization and allowed labeling of the coronary vessels, thereby defining the morphogenic processes involved in formation of collateral circulations. The results show that the heart consistently responds to infarcts with angiogenesis at 1d post-treatment (PT) that undergoes transition into vascular remodeling at 7d PT with complete remodeling at 14d PT. The vascular remodeling appears to mitigate any net increase in perfusion that may be achieved early in coronary angiogenesis. The results suggest that therapeutic approaches need to shift from an exclusive focus on stimulating angiogenesis to include modulation of vascular remodeling for increased long-term myocardial perfusion.
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