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Updated: Nov 17, 2025
Cell-free Biochemical Fluorometric Enzymatic Assay for High-throughput Measurement of Lipid Peroxidation in High Density Lipoprotein
Published on: October 12, 2017
JCL roundtable: Lipids and inflammation in atherosclerosis.
Karin E Bornfeldt1, MacRae F Linton2, Edward A Fisher3
1University of Washington Medicine Diabetes Institute, Division of Metabolism, Endocrinology and Nutrition, Departments of Medicine and Laboratory Medicine and Pathology, University of Washington, Seattle, WA, USA.
Atherosclerosis pathogenesis involves low-density lipoproteins, triglyceride-rich lipoprotein remnants, and inflammation. New insights into microRNAs and cellular processes promise targeted therapies for residual cardiovascular risk.
Area of Science:
- Lipidology
- Cardiovascular Pathogenesis
- Molecular Biology
Background:
- Atherosclerosis primarily affects the intimal layer of large arteries.
- Current lipidology research focuses on mitigating atherosclerosis effects.
- Understanding atherogenesis is key to developing new therapies.
Purpose of the Study:
- To discuss the current understanding of atherosclerosis pathogenesis.
- To highlight emerging factors promoting atherogenesis.
- To explore the role of inflammation and microRNAs in atherosclerosis.
Main Methods:
- Expert roundtable discussion among leading researchers.
- Review of current literature on lipoprotein metabolism and inflammation.
- Integration of findings on cellular processes and gene regulation.
Main Results:
- Low-density lipoprotein retention in arterial intima is a key factor (response-to-retention hypothesis).
- Triglyceride-rich lipoprotein remnants, particularly apolipoprotein C-III, promote atherogenesis.
- Inflammation's role is clarified through leukocyte recruitment, efferocytosis, and crystal formation.
- MicroRNAs emerge as critical regulators of lipoprotein and inflammation biology.
Conclusions:
- Atherosclerosis is a complex process involving lipoproteins, inflammation, and gene regulation.
- Emerging research on microRNAs and cellular mechanisms offers new therapeutic avenues.
- Future treatments may target residual cardiovascular risk factors like obesity and diabetes.
