Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Videos

Pathogenesis of atherosclerosis

Z A Massy1, W F Keane

  • 1Department of Medicine, University of Minnesota Medical School, Minneapolis, USA.

Seminars in Nephrology
|January 1, 1996
PubMed
Summary
This summary is machine-generated.

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Response to the Letter to the Editor Entitled "Optimizing Furosemide Use in Advanced CKD: Balancing Risks and Benefits".

Kidney international reports·2025
Same author

Obesity phenotype and patient-reported outcomes in moderate and severe chronic kidney disease: a cross-sectional study from the CKD-REIN cohort study.

Quality of life research : an international journal of quality of life aspects of treatment, care and rehabilitation·2019
Same author

Mortality due to bleeding, myocardial infarction and stroke in dialysis patients.

Journal of thrombosis and haemostasis : JTH·2018
Same author

TWEAK favors phosphate-induced calcification of vascular smooth muscle cells through canonical and non-canonical activation of NFκB.

Cell death & disease·2016
Same author

The uses and abuses of Vitamin D compounds in chronic kidney disease-mineral bone disease (CKD-MBD).

Seminars in nephrology·2014
Same author

The relationships between serum sclerostin, bone mineral density, and vascular calcification in rheumatoid arthritis.

The Journal of clinical endocrinology and metabolism·2014
Same journal

Current Options for Kidney Protection: Are Renin-Angiotensin System Inhibitors Still Relevant?

Seminars in nephrology·2026
Same journal

Proposed Role for Quantitative Podocyturia as a Clinical Marker of Systemic Endothelial Injury: Implications for Cardiovascular Disease and Longevity.

Seminars in nephrology·2026
Same journal

Kidney Protection Options in 2025: Are Renin-Angiotensin System Inhibitors Still Needed?

Seminars in nephrology·2026
Same journal

From Nephron Number to Global Health.

Seminars in nephrology·2026
Same journal

Chronic Kidney Disease Progression Mechanisms: Why They Matter in an Era of Novel Kidney Protective Therapies.

Seminars in nephrology·2026
Same journal

Of Diuretics, Transporters, and Mechanisms of Hypertension.

Seminars in nephrology·2026
See all related articles

Atherosclerosis involves arterial wall injury and repair, leading to plaque buildup. This process, characterized by lipid-laden macrophages and smooth muscle cells, can obstruct blood flow.

Area of Science:

  • Cardiovascular Biology
  • Pathology
  • Immunology

Background:

  • Atherosclerosis is a complex arterial disease driven by interactions between injury and repair mechanisms.
  • Endothelial dysfunction initiates a cascade involving monocyte recruitment, smooth muscle cell proliferation, and matrix protein synthesis.

Purpose of the Study:

  • To elucidate the cellular and molecular mechanisms underlying atherosclerosis development and progression.
  • To detail the histopathological changes from early fatty streaks to advanced obstructive lesions.

Main Methods:

  • The study describes the pathological process based on established histopathological findings.
  • It integrates knowledge of cellular interactions, growth factor signaling, and lipid accumulation.

Related Experiment Videos

Main Results:

  • Endothelial injury triggers monocyte recruitment, transformation into lipid-laden macrophages (foam cells), and formation of fatty streaks.
  • Atherosclerotic lesion progression involves layered accumulation of smooth muscle cells and macrophages.
  • Advanced lesions narrow arterial lumen, impeding blood flow and potentially causing occlusion.

Conclusions:

  • Atherosclerosis is a progressive disease initiated by endothelial injury and characterized by inflammatory cell infiltration and lipid deposition.
  • The accumulation of foam cells and smooth muscle cells leads to significant arterial narrowing and reduced blood flow.
  • Understanding these mechanisms is crucial for developing therapeutic strategies against atherosclerosis.