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Mechanisms that regulate macrophage burden in atherosclerosis
1From the Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO. grandolph@path.wustl.edu.
Abstract:
Mononuclear phagocytes (MPs) relevant to atherosclerosis include monocytes, macrophages, and dendritic cells. A decade ago, studies on macrophage behavior in atherosclerotic lesions were often limited to quantification of total macrophage area in cross-sections of plaques. Although technological advances are still needed to examine plaque MP populations in an increasingly dynamic and informative manner, innovative methods to interrogate the biology of MPs in atherosclerotic plaques developed in the past few years point to several mechanisms that regulate the accumulation and function of MPs within plaques. Here, I review the evolution of atherosclerotic plaques with respect to changes in the MP compartment from the initiation of plaque to its progression and regression, discussing the roles that recruitment, proliferation, and retention of MPs play at these different disease stages. Additional work in the future will be needed to better distinguish macrophages and dendritic cells in plaque and to address some basic unknowns in the field, including just how cholesterol drives accumulation of macrophages in lesions to build plaques in the first place and how macrophages as major effectors of innate immunity work together with components of the adaptive immune response to drive atherosclerosis. Answers to these questions are sought with the goal in mind of reversing disease where it exists and preventing its development where it does not.
Insights
Mononuclear phagocytes (MPs) are key to atherosclerosis. Recent advances reveal mechanisms regulating MP accumulation and function in plaques, offering new avenues for disease reversal and prevention.
Area of Science:
- Cardiovascular Biology
- Immunology
- Atherosclerosis Research
Background:
- Mononuclear phagocytes (MPs), including monocytes, macrophages, and dendritic cells, are central to atherosclerosis.
- Historically, macrophage quantification in atherosclerotic lesions was limited.
- Technological progress is enhancing the study of dynamic MP populations within plaques.
Purpose of the Study:
- To review the evolution of atherosclerotic plaques focusing on changes in the MP compartment.
- To discuss the roles of MP recruitment, proliferation, and retention in plaque development, progression, and regression.
- To highlight current knowledge gaps and future research directions in MP biology and atherosclerosis.
Main Methods:
- Review of recent literature and innovative methods for interrogating MP biology in atherosclerotic plaques.
- Analysis of MP compartment dynamics from plaque initiation to regression.
- Identification of mechanisms regulating MP accumulation and function.
Main Results:
- Innovative methods have uncovered mechanisms governing MP accumulation and function in atherosclerotic plaques.
- The roles of MP recruitment, proliferation, and retention vary across different stages of plaque evolution.
- Key questions remain regarding cholesterol's role in macrophage accumulation and the interplay between innate and adaptive immunity in driving atherosclerosis.
Conclusions:
- Understanding MP dynamics is crucial for comprehending atherosclerosis.
- Future research should focus on distinguishing macrophage and dendritic cell roles and elucidating cholesterol-driven accumulation.
- Investigating the innate-adaptive immune crosstalk in atherosclerosis is essential for developing therapeutic strategies.
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