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Published on: September 26, 2018
Plaque angiogenesis and its relation to inflammation and atherosclerotic plaque destabilization
Margreet R de Vries1, Paul H A Quax
1Department of Surgery, Einthoven Laboratory for Experimental Vascular Medicine, Leiden University Medical Center, Leiden, The Netherlands.
Insights
Plaque angiogenesis, linked to inflammation and intraplaque hemorrhage, drives atherosclerosis vulnerability. Understanding this process offers new therapeutic targets for cardiovascular disease.
Area of Science:
- Cardiovascular Research
- Pathology
- Angiogenesis Research
Background:
- Plaque angiogenesis is closely linked to inflammation, intraplaque hemorrhage (IPH), and plaque vulnerability.
- Hypoxia is a primary driver of plaque angiogenesis, though the exact mechanisms remain partially understood.
- Immature neovessels contribute to IPH, increasing inflammatory cell infiltration within atherosclerotic plaques.
Purpose of the Study:
- To review recent literature on plaque angiogenesis in relation to inflammation and plaque destabilization.
- To explore the potential of plaque angiogenesis as a monitoring tool for atherosclerosis.
- To identify plaque angiogenesis as a potential therapeutic target for cardiovascular disease.
Main Methods:
- Review of histopathologic and imaging studies on plaque angiogenesis and vulnerability.
- Analysis of experimental models that mimic human atherosclerosis features.
- Examination of emerging imaging techniques for detecting plaque angiogenesis.
Main Results:
- Histopathologic studies confirm a strong correlation between plaque angiogenesis, IPH, plaque vulnerability, and cardiovascular events.
- Experimental models aid in understanding the mechanisms underlying plaque vulnerability.
- New imaging technologies enable the detection of plaque angiogenesis and vulnerability.
Conclusions:
- Plaque angiogenesis, IPH, and inflammation are key contributors to atherosclerotic plaque vulnerability.
- Current histopathologic, imaging, and experimental studies provide valuable insights but require further mechanistic understanding.
- Elucidating the underlying mechanisms is crucial for developing effective therapies for at-risk patients.
Purpose Of Review:
The review discusses the recent literature on plaque angiogenesis and its relation to inflammation and plaque destabilization. Furthermore, it discusses how plaque angiogenesis can be used to monitor atherosclerosis and serve as a therapeutic target.
Recent Findings:
Histopathologic studies have shown a clear relationship between plaque angiogenesis, intraplaque hemorrhage (IPH), plaque vulnerability, and cardiovascular events. Hypoxia is a main driver of plaque angiogenesis and the mechanism behind angiogenesis is only partly known. IPH, as the result of immature neovessels, is associated with increased influx of inflammatory cells in the plaques. Experimental models displaying certain features of human atherosclerosis such as plaque angiogenesis or IPH are developed and can contribute to unraveling the mechanism behind plaque vulnerability. New imaging techniques are established, with which plaque angiogenesis and vulnerability can be detected. Furthermore, antiangiogenic therapies in atherosclerosis gain much attention.
Summary:
Plaque angiogenesis, IPH, and inflammation contribute to plaque vulnerability. Histopathologic and imaging studies together with specific experimental studies have provided insights in plaque angiogenesis and plaque vulnerability. However, more extensive knowledge on the underlying mechanism is required for establishing new therapies for patients at risk.
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