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TAM receptors and their ligand-mediated activation: Role in atherosclerosis
Bishuang Cai1, Canan Kasikara2
1Division of Liver Diseases, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, NY, United States.
Abstract:
TAM family tyrosine kinase receptors including Tyro3, Axl, and MerTK are the key efferocytosis receptors presenting on antigen-presenting cell that mediate the clearance of apoptotic cells. They are thought to regulate inflammatory diseases by modulating inflammatory response and efferocytosis. Recent studies have revealed novel roles of TAM receptors in the biosynthesis of specialized pro-resolving mediators (SPMs) and inflammation resolution. In this chapter, we discuss the central roles of TAM signaling in atherosclerosis focusing on their regulation in efferocytosis and inflammation resolution and highlight the unique therapeutic potential of SPMs in blocking the progression of atherosclerosis.
Insights
TAM receptors (Tyro3, Axl, MerTK) are crucial for clearing apoptotic cells and resolving inflammation. Targeting these receptors and specialized pro-resolving mediators (SPMs) offers therapeutic potential for atherosclerosis.
Area of Science:
- Immunology
- Molecular Biology
- Cardiovascular Research
Background:
- TAM family tyrosine kinase receptors (Tyro3, Axl, MerTK) are key mediators of efferocytosis.
- These receptors play a role in regulating inflammatory responses and diseases.
- Emerging evidence highlights their involvement in inflammation resolution and specialized pro-resolving mediator (SPM) biosynthesis.
Purpose of the Study:
- To discuss the central roles of TAM signaling in atherosclerosis.
- To focus on TAM receptor regulation of efferocytosis and inflammation resolution.
- To highlight the therapeutic potential of SPMs in atherosclerosis.
Main Methods:
- Review of recent studies on TAM signaling.
- Analysis of TAM receptor function in efferocytosis.
- Exploration of SPM roles in inflammation resolution.
Main Results:
- TAM receptors are critical for efferocytosis by antigen-presenting cells.
- TAM signaling modulates inflammatory responses and contributes to inflammation resolution.
- SPMs are involved in the regulation of atherosclerosis progression.
Conclusions:
- TAM signaling is central to efferocytosis and inflammation resolution in atherosclerosis.
- Targeting TAM receptors and SPMs presents a promising therapeutic strategy for blocking atherosclerosis progression.
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