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Assessing Therapeutic Angiogenesis in a Murine Model of Hindlimb Ischemia
Published on: June 8, 2019
A critical review of clinical arteriogenesis research
Niels van Royen1, Jan J Piek, Wolfgang Schaper
1Department of Cardiology, Academic Medical Center, University of Amsterdam, Amsterdam, the Netherlands. n.vanroyen@amc.uva.nl
Insights
Human hearts possess a robust collateral network that expands when coronary arteries close. This process, arteriogenesis, involves circulating cells and offers targets for new therapies.
Area of Science:
- Cardiovascular Research
- Vascular Biology
- Regenerative Medicine
Background:
- Human hearts have an extensive pre-existing collateral network, demonstrated through post-mortem angiographic studies.
- Collateral vessels enlarge upon coronary artery closure, challenging the 'end artery' concept and forming the basis of arteriogenesis.
- Circulating cells, particularly monocytes, play a crucial role in collateral vessel maturation by secreting essential factors.
Purpose of the Study:
- To review the current understanding of arteriogenesis in the human heart.
- To highlight the role of monocytes and growth factors in collateral circulation development.
- To discuss the challenges and future directions in stimulating arteriogenesis therapeutically.
Main Methods:
- Review of historical post-mortem angiographic studies.
- Analysis of experimental studies on collateral circulation and monocyte involvement.
- Discussion of clinical studies and the use of collateral flow index for assessing arteriogenesis.
- Application of a bedside-to-bench approach using patient data to identify therapeutic targets.
Main Results:
- Pre-existing collateral vessels in the human heart actively enlarge following coronary artery obstruction.
- Monocytes are key players in the arteriogenesis process, contributing to vessel wall proliferation and maturation.
- Clinical studies on arteriogenesis stimulation have shown limited success, necessitating novel approaches.
- Intracoronary collateral flow index aids in detecting arteriogenesis effects and identifying patients with impaired responses.
Conclusions:
- Arteriogenesis is a critical adaptive mechanism in the human heart involving remodeling of pre-existing vessels.
- Understanding the cellular and molecular mechanisms of arteriogenesis is vital for developing effective treatments for ischemic heart disease.
- Identifying patients with defective arteriogenesis and characterizing their molecular profiles can lead to new therapeutic strategies.
Abstract:
In human hearts, an extensive pre-existing collateral network is present. This was shown unequivocally some 50 years ago in a series of very detailed post-mortem angiographic studies. In these studies, it was also observed that the pre-existent collateral vessels enlarge upon closure of an epicardial coronary artery, resulting in large collateral conduit arteries, in sharp contrast to earlier claims that human coronary arteries are functional end arteries. These insights still form the basis for the concept of arteriogenesis as positive remodeling of pre-existent arteriolar connections. Subsequent experimental studies disclosed the putative role of circulating cells, especially monocytes, which invade the proliferating vessel wall and secrete growth factors, degrading enzymes and survival factors that are required for the development of a mature collateral circulation. Experimental stimulation of arteriogenesis is feasible but to date a relatively low number of clinical studies, with no or limited success, have been performed. The use of intracoronary derived collateral flow index can increase the sensitivity to detect the effects of pharmacological compounds on arteriogenesis, which is important in first proof-of-principle studies. These invasive measurements also allow the detection of patients with an innate defect in their arteriogenic response to coronary obstruction. In a reversed bedside-to-bench approach, the characterization of ribonucleic acid and protein expression patterns in these patients generated new targets for therapeutic arteriogenesis.
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