Macrophages and immune cells in atherosclerosis: recent advances and novel concepts

Area of Science:

• Cardiovascular Biology
• Immunology
• Pathology

Background:

• Atherosclerosis, driven by inflammation, causes heart attack and stroke, leading causes of death.
• Macrophage accumulation in atherosclerotic plaques is a key feature of disease progression.
• Adaptive immune responses significantly influence inflammatory processes in atherosclerosis.

Purpose of the Study:

• To review recent advances in understanding inflammatory processes in atherosclerosis.
• To discuss novel mechanisms of immune cell involvement in plaque development.
• To highlight emerging evidence challenging traditional views on macrophage accumulation.

Main Methods:

• Literature review of recent research on atherosclerosis and inflammation.
• Analysis of studies on immune cell subsets and their roles in plaque formation.
• Synthesis of evidence regarding macrophage proliferation and transdifferentiation in lesions.

Main Results:

• Macrophage accumulation may occur via onsite proliferation and smooth muscle cell transdifferentiation, not solely monocyte recruitment.
• Previously unrecognized roles of plasmacytoid dendritic cells, innate response activator B cells, and CD8(+) T cells in atherosclerosis have been identified.
• Novel mechanisms involving regulatory T cells and natural killer T cells in lesion development have emerged.

Conclusions:

• Inflammatory processes, particularly macrophage dynamics and diverse immune cell subsets, are critical in atherosclerosis.
• Recent findings necessitate a revised understanding of macrophage accumulation and immune cell contributions to atherosclerotic plaque progression.
• Further research into these inflammatory pathways may reveal new therapeutic targets for cardiovascular diseases.