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An In Vivo Duo-color Method for Imaging Vascular Dynamics Following Contusive Spinal Cord Injury
Published on: December 31, 2017
Trail and vascular injury
Jose L Martin-Ventura1, Begona Munoz-Garcia, Jesus Egido
1Vascular Research Lab, Fundacion Jimenez Diaz, Autonoma University, Madrid, Spain. jlmartin@fjd.es
Insights
Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) may promote vascular inflammation and cell death in atherosclerosis. Plasma levels of TRAIL and osteoprotegerin (OPG) are being investigated as potential markers for vascular injury.
Area of Science:
- Cardiovascular biology
- Immunology
- Molecular medicine
Background:
- Cardiovascular diseases are a leading cause of death, driven by atherosclerosis, characterized by arterial wall thickening and atheromatous plaque formation.
- Key atherogenesis mechanisms include lipoprotein retention, endothelial activation, smooth muscle cell proliferation, macrophage infiltration, and apoptosis.
- Members of the tumor necrosis factor (TNF) family, including TNF-related apoptosis-inducing ligand (TRAIL) and its receptors (TRAIL-Rs, OPG), are found in atherosclerotic plaques.
Purpose of the Study:
- To review the role of TRAIL and its receptors in the mechanisms of atherothrombosis.
- To discuss the controversial effects of TRAIL on vascular cell inflammation and apoptosis.
- To explore the potential of plasma TRAIL and OPG levels as biomarkers for vascular injury.
Main Methods:
- Literature review of studies on TRAIL and its receptors in atherogenesis.
- Analysis of in vivo studies investigating TRAIL's role in vascular injury.
- Examination of research on soluble TNF-superfamily members in human plasma.
Main Results:
- TRAIL and its receptors are present in human atherosclerotic plaques.
- Data on TRAIL's effects on vascular cell inflammation and apoptosis remain controversial.
- Recent in vivo studies suggest TRAIL may have pro-inflammatory and pro-apoptotic effects in vascular injury.
Conclusions:
- TRAIL and its receptors are implicated in atherothrombosis.
- Further research is needed to clarify TRAIL's precise role in vascular inflammation and apoptosis.
- Plasma levels of TRAIL and OPG may serve as potential biomarkers for vascular injury.
Abstract:
Cardiovascular diseases are the leading cause of mortality in the Western world. The underlying pathological process is a thickening of the arterial wall due to the formation of atheromatous plaques which contain a lipid core covered by a fibrous cap. The main mechanisms involved in atherogenesis are: lipoprotein retention, endothelial cell activation, vascular smooth muscle cell proliferation, macrophage infiltration, proteolytic injury, neovascularization and apoptosis. Different members of the tumor necrosis factor family (TNF) of proteins have been detected in human atherosclerotic plaques, among these are TNF-related apoptosis-inducing ligand (TRAIL) and its receptors (TRAIL-Rs and osteoprotegerin, OPG). In this review, the involvement of TRAIL and its receptors in the mechanisms underlying atherothrombosis is reviewed. In this respect, there are still some controversial data on the effects of TRAIL on inflammation and apoptosis of vascular cells. However, recent in vivo studies have suggested a potential proinflammatory and proapoptotic role of TRAIL in vascular injury. In addition, soluble forms of the TNF-superfamily can be released extracellularly and have been detected in human plasma. For this reason, we different studies evaluating the potential use of TRAIL and OPG plasma levels as markers of vascular injury are discussed.
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