
Accumulation of classical monocytes is imperative for the progression of atherosclerosis. Hence, therapeutic interference with mechanisms of lesional monocyte recruitment, the primary mechanism controlling macrophage accumulation, may allow for targeting atheroprogression and its clinical complications. Here, we review the important role of classical monocytes in atheroprogression as well as their routes of arterial recruitment. We specifically highlight the role of cell adhesion molecules as well as of platelet-derived chemokines and neutrophil-borne alarmins.
Blood Platelets, Neutrophils, Macrophages, Arteries, Atherosclerosis, Cell Movement, Disease Progression, Animals, Humans, Molecular Targeted Therapy, Chemokines, Cell Adhesion Molecules
Blood Platelets, Neutrophils, Macrophages, Arteries, Atherosclerosis, Cell Movement, Disease Progression, Animals, Humans, Molecular Targeted Therapy, Chemokines, Cell Adhesion Molecules
| selected citations These citations are derived from selected sources. This is an alternative to the "Influence" indicator, which also reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically). | 15 | |
| popularity This indicator reflects the "current" impact/attention (the "hype") of an article in the research community at large, based on the underlying citation network. | Top 10% | |
| influence This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically). | Average | |
| impulse This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network. | Top 10% |
