Related Experiment Video
Updated: May 8, 2026
06:43
Quantitative Analysis and Characterization of Atherosclerotic Lesions in the Murine Aortic Sinus
Published on: December 7, 2013
Proliferating macrophages prevail in atherosclerosis.
1Department of Pathology and Immunology at Washington University School of Medicine, St. Louis, Missouri, USA.
Nature Medicine
|September 10, 2013
Summary
Macrophage accumulation in atherosclerotic plaques is driven by local proliferation, not circulating monocyte recruitment. This finding impacts our understanding of atherosclerosis development and inflammation.
Area of Science:
- Cardiovascular Research
- Immunology
- Pathology
Background:
- Atherosclerosis involves chronic inflammation and macrophage accumulation in arterial walls.
- Macrophages play a critical role in the development and progression of atherosclerotic lesions.
Discussion:
- This study investigates the source of macrophages within atherosclerotic plaques.
- It challenges the traditional view that circulating monocytes are the primary contributors.
Key Insights:
- Macrophage accumulation in atherosclerotic plaques is primarily due to local proliferation within the plaque.
- Recruitment of monocytes from the bloodstream is a less significant factor in plaque macrophage expansion.
Outlook:
- Understanding local proliferation mechanisms could reveal novel therapeutic targets for atherosclerosis.
- Further research is needed to explore the signaling pathways driving macrophage proliferation in plaques.
Related Concept Videos
01:38Inflammation
Overview
01:30Atherosclerosis I: Introduction
Atherosclerosis is a progressive disorder characterized by the buildup of plaques on the arterial inner wall, causing them to narrow and harden over time. These plaques comprise lipids, calcium, blood components, carbohydrates, and fibrous tissue. The process primarily affects the intima of large and medium-sized arteries, reducing blood flow in any artery.Etiology and risk factorsThe cause of atherosclerosis is multifactorial, involving a complex interplay among endothelial injury, lipid...
01:26Coronary Artery Disease II: Pathophysiology
Coronary Artery Disease (CAD) originates from a series of events that impair the function of coronary arteries, the blood vessels responsible for delivering oxygen-rich blood to the heart muscle. The pathophysiology of CAD is closely linked to atherosclerosis, a chronic inflammatory and lipid-driven condition affecting the vascular endothelium.1. Endothelial DamageThe process begins with damage to the vascular endothelium, which serves as a protective barrier between the blood and the vessel...
01:12Chronic Inflammation: Introduction
Chronic inflammation is a prolonged, dysregulated immune response that persists for weeks to years when the inciting stimulus is difficult to eradicate or when self‑antigens drive ongoing reactivity. Morphologically, it is defined by mononuclear cell infiltration, progressive tissue destruction, and concurrent attempts at healing via angiogenesis and fibrosis. Compared with acute inflammation, edema is less prominent while cellular infiltration predominates; triggers include persistent...
01:30Peripheral Artery Disease I: Introduction
Peripheral artery disease (PAD) predominantly results from atherosclerosis, which involves the accumulation of fatty deposits, or plaques, within the walls of arteries. This causes them to narrow and harden, significantly reducing blood flow. PAD predominantly affects the legs, particularly the arteries supplying the thighs and calves. In rare cases, it may involve other arteries, including those in the arms.Etiology of PAD:The principal cause of PAD is atherosclerosis, which results from fatty...
01:17Phagocytosis of Apoptotic Cells
Cells undergoing apoptosis form apoptotic bodies that must be removed immediately to prevent inflammation, autoimmune diseases, and necrosis. Phagocytosis is carried out by professional phagocytes such as macrophages or immature dendritic cells. Non-professional phagocytes such as epithelial cells and fibroblasts also take part in this process; however, they are not as effective as professional phagocytes.
Normal cells contain receptors that prevent them from being recognized by phagocytes.
Normal cells contain receptors that prevent them from being recognized by phagocytes.