Unraveling the significance of innate inflammation in vascular disease
- PMID: 40255209
- DOI: 10.1080/08830185.2025.2489346
Unraveling the significance of innate inflammation in vascular disease
Abstract
Atheroma formation is initiated by the activation of endothelial and smooth muscle cells, as well as immune cells, including neutrophils, lymphocytes, monocytes, macrophages, and dendritic cells. Monocytes, macrophages, and neutrophils are the innate immune cells that provide a rapid initial line of defence against vascular disease. These cells have a short lifespan and cannot retain memories, making them potential therapeutic targets for the inflammatory process associated with atherosclerosis. In addition, macrophages comprise the majority of vessel wall infiltrates and are, therefore, implicated in all stages of atherosclerosis progression. Neutrophils are the most common type of leukocyte found in circulation, and their high levels of matrix-degrading protease explain their significance in fibrous cap destabilization. However, the activation of immune cells becomes more complex by various microenvironmental stimuli and cytokines, which ultimately transform immune cells into their pro-inflammatory state. Different types of macrophage subsets with distinct functions in inflammation, such as M1 macrophages, cause an increase in pro-inflammatory cytokines and produce reactive oxygen species and nitric oxide, further worsening the disease. This review aims to shed light on immune-mediated inflammation in cardiovascular disease by focusing on the role of macrophage subsets in vascular inflammation and plaque stability, as well as the interaction between neutrophils and monocyte-macrophages.
Keywords: Atherosclerosis; foam cells; innate inflammation; macrophages; plaque stability.
Plain language summary
Cardiovascular disease is a leading cause of global mortality. The onset of this condition frequently occurs due to vascular inflammation, which can be initiated at an early age. The body’s immune system, specifically phagocytic cells such as monocytes, macrophages, and neutrophils, significantly contributes to this process. These cells typically aid in combating infections, but they can also cause complications in our blood vessels, ultimately resulting in heart disease.Our review examines the role of these immune cells in the formation of plaques in our arteries, a condition called atherosclerosis that can result in heart attacks and strokes. Macrophages are a cellular type that engulfs and digests harmful cholesterol in our blood vessels. However, they can become overwhelmed and transform into foam cells, which play a significant role in the formation of these hazardous plaques. Neutrophils, a different category of immune cells, might exacerbate the condition by increasing the likelihood of plaque rupture, leading to a heart attack. Additionally, we discuss the varying behaviours of these cells in response to signals from their environment, which can either exacerbate or alleviate inflammation, alongside the existing anti-inflammatory strategies aimed at reducing inflammation associated with immune responses. A more profound understanding of these mechanisms may pave the way for identifying innovative treatment or prevention strategies for heart disease, specifically targeting these cells and their functions.Essentially, our bodies’ protective mechanisms can occasionally malfunction and result in the development of cardiac disease. Gaining further knowledge about this issue can facilitate the development of novel therapies to maintain the optimal functioning of our cardiovascular system.
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