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Published on: August 20, 2019
Endothelial dysfunction sustains immune response in atherosclerosis: potential cause for ineffectiveness of
Shamima Akhtar1, Alpana Sharma1
1Department of Biochemistry, All India Institute of Medical Sciences (AIIMS), New Delhi, India.
Insights
Vascular endothelial dysfunction (ED) drives atherosclerosis and related diseases. This review explores how ED activates the immune system and questions the effectiveness of current drugs in reversing these immune responses.
Area of Science:
- Cardiovascular Science
- Immunology
- Endothelial Biology
Background:
- Vascular endothelial dysfunction (ED) is central to atherosclerosis, leading to ischemia, myocardial infarction, stroke, and peripheral arterial disease.
- Risk factors like hypercholesterolemia, hypertension, hyperhomocystenemia, and inflammation trigger ED and systemic immune responses.
- Current atherosclerosis drugs manage risk factors and suppress immune activation, but their efficacy in treating ED remains uncertain.
Purpose of the Study:
- To discuss how pathological molecules and processes in ED activate innate and adaptive immunity.
- To evaluate the potential of current drugs in reversing immune activation driven by ED, even without traditional risk factors.
Main Methods:
- Review of literature focusing on mechanisms of endothelial activation.
- Analysis of endothelial microparticles, mechanically stretched endothelial cells, endothelial mesenchymal transition, and endothelial glycocalyx shedding.
- Discussion of immune system activation in the context of ED.
Main Results:
- Pathological processes in ED can activate immune responses independently of cardiovascular risk factors.
- Specific endothelial changes like microparticle release and glycocalyx shedding contribute to immune activation.
- The role of current atherosclerosis medications in reversing ED-induced immune responses is questionable.
Conclusions:
- Endothelial dysfunction is a significant driver of immune system activation in atherosclerosis.
- Further research is needed to determine if current treatments can reverse ED-related immune responses.
- Targeting specific endothelial pathways may offer new therapeutic strategies for atherosclerosis.
Abstract:
Vascular endothelial dysfunction (ED) forms the cornerstone in the development of atherosclerotic lesions that clinically manifest as ischemia, myocardial infarction, stroke or peripheral arterial disease. ED can be triggered by various risk factors including hypercholesterolemia, hypertension, hyperhomocystenemia and chronic low-grade inflammation. These risk factors also activate immune response systemically. Current drugs used for managing atherosclerosis not only aid in subsiding the risk factor but also suppress the immune activation. Nonetheless, their effectiveness in treating ED is still questionable. Here, we discuss how pathologic molecules and processes pertaining to ED can activate innate and adaptive arms of the immune system leading to disease progression even in the absence of cardiovascular risk factors and the potential of the current drugs, used in the management of atherosclerotic patients, in reversing them. We mainly focus on activated endothelium, endothelial microparticles, mechanically stretched endothelial cells, endothelial mesenchymal transition and endothelial glycocalyx sheds.
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