Abstract
Atherosclerosis is a chronic progressive disease that involves damage to the intima, inflammatory cell recruitment and the accumulation of lipids followed by calcification and plaque rupture. Inflammation is considered a key mediator of many events during the development and progression of the disease. Various types of inflammatory cells are reported to be involved in atherosclerosis. In the present paper, we discuss the involved inflammatory cells, their characteristic and functional significance in the development and progression of atherosclerosis. The detailed understanding of the role of all these cells in disease progression at different stages sheds more light on the subject and provides valuable insights as to where and when therapy should be targeted.
Highlights
IntroductionNumerous pathological studies suggest that macrophage abundance from an early stage of atherosclerosis to late stages, i.e., from fatty streak lesions to the fibrous plaques, indicates the critical role of these cells in the development and progression of the disease [13,14]
The development of diagnostics and prognostics with advanced techniques explores the treatment of atherosclerosis
By understanding the main path that ends with foam cell accumulation and calcification, which is the catalyst for creating an environment prone to rupture, the smaller pathways of inhibition and promotion can be investigated in more depth
Summary
Numerous pathological studies suggest that macrophage abundance from an early stage of atherosclerosis to late stages, i.e., from fatty streak lesions to the fibrous plaques, indicates the critical role of these cells in the development and progression of the disease [13,14]. These lipid-laden macrophages play a key role in plaque rupture by producing various pro-inflammatory mediators and reactive oxygen species (ROS) [15].
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