Atherosclerotic Lesion Biology
Atherosclerotic Lesion Biology - Related Videos
05:51
A Human Ex Vivo Atherosclerotic Plaque Model to Study Lesion Biology
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Cited by 13 •
2014
Atherosclerosis is a chronic inflammatory process. This manuscript illustrates an easy to use ex vivo model to investigate fresh carotid or coronary artery plaques. The ex vivo model allows for the investigation of potential substances on the inflammatory milieu in human atherosclerotic lesions and results can be analyzed by various methods.
06:43
Quantitative Analysis and Characterization of Atherosclerotic Lesions in the Murine Aortic Sinus
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Cited by 51 •
2013
We describe procedures to quantify and characterize atherosclerotic lesions in mouse models using precision sectioning of the aortic sinus and ascending aorta combined with histochemical and immunohistochemical analysis.
07:49
Isolation and Analysis of Aortic Arch and Root Lesions in an Atherosclerotic Mouse Model
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2025
This protocol provides a comprehensive methodology for the quantitative analysis of atherosclerotic plaques to facilitate more in-depth research into the mechanisms and progression of atherosclerosis.
11:45
Generation and 3-Dimensional Quantitation of Arterial Lesions in Mice Using Optical Projection Tomography
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Cited by 5 •
2015
Ex vivo analysis of arterial lesions from animal models of cardiovascular disease classically relies on histological and immunohistochemical techniques. These provide 2-dimensional measurements in 3-dimensional lesions. This manuscript describes the generation of arterial lesions for quantitative analysis in 3-dimensions using optical projection tomography.
09:06
Quantitative Analysis of Cellular Composition in Advanced Atherosclerotic Lesions of Smooth Muscle Cell Lineage-Tracing Mice
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Cited by 1 •
2019
We propose a standardized protocol to characterize the cellular composition of late-stage murine atherosclerotic lesions including systematic methods of animal dissection, tissue embedding, sectioning, staining, and analysis of brachiocephalic arteries from atheroprone smooth muscle cell lineage tracing mice.
FAQs
Endothelial dysfunction makes the arterial lining more permissive to low-density lipoprotein retention in the intima, the innermost arterial layer. Once retained, these lipids can undergo modification and promote recruitment of circulating monocytes. This early sequence links vascular-lining injury to local lipid accumulation and establishes conditions that support subsequent inflammatory lesion development.
Recruited monocytes enter the arterial wall and become macrophages, which accumulate cholesterol. Their lipid loading contributes to the formation of lipid-rich regions and sustains local inflammation. This cellular response is important because it connects retained, modified lipids with the broader tissue changes that influence lesion growth and the later behavior of the plaque.
Smooth muscle cell changes and fibrous-cap formation are structural components of lesion evolution. The fibrous cap helps characterize how a plaque is organized, while changes in smooth muscle cells reflect remodeling of the arterial wall. Studying these features helps explain why some lesions primarily narrow the vessel whereas others may become structurally weak.
Lesions can produce complications through two related but distinct consequences. Progressive plaque accumulation may narrow the artery and restrict its internal passage. Alternatively, weakening of the plaque can increase the likelihood of rupture, followed by thrombosis. These outcomes connect lesion structure and progression with clinical events such as myocardial infarction and stroke.
This field can reveal cellular and molecular features associated with lesion development, progression, and instability. Those features support biomarker discovery, which may improve assessment of cardiovascular risk, and help identify processes suitable for therapeutic development. The resulting knowledge connects observations within arterial tissue to clinically relevant prediction and treatment strategies.
Risk assessment benefits from distinguishing the presence of lipid-rich lesions from features associated with progression or weakening. Cellular inflammation, cholesterol accumulation, smooth muscle cell changes, and fibrous-cap formation provide biologically meaningful context for interpreting lesion behavior. Studying these factors may help relate arterial-wall pathology to the likelihood of thrombosis, myocardial infarction, or stroke.