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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.
Insights
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.
Abstract:
Clinical effort in lipidology focuses largely on mitigating effects of atherosclerosis, a pathologic process localized to the intimal layer of larger arteries. This JCL Roundtable brings together 3 leading researchers to discuss the current understanding of pathogenesis in atherosclerosis. We begin by recognizing that low density lipoprotein concentrations in arterial intima far exceed concentrations in other connective tissues, consistent with the response-to-retention hypothesis of atherogenesis. High density lipoproteins facilitate reverse cholesterol transport and also have antioxidant and anti-inflammatory roles. New evidence points to remnants of triglyceride-rich lipoproteins as promoters of atherogenesis, highlighted by deleterious effects of apolipoprotein C-III. The multifaceted role of inflammation is becoming clearer through discoveries related to leukocyte recruitment, efferocytosis, resolution of inflammation, and crystal formation. MicroRNAs represent a new, complex mode of gene regulation bearing on lipoprotein and inflammation biology. Progress in understanding atherosclerosis portends a future in which residual risk related to obesity, diabetes, and other factors will yield to new targeted therapies.
