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Updated: May 1, 2026

A Human Ex Vivo Atherosclerotic Plaque Model to Study Lesion Biology
Published on: May 6, 2014
Atherosclerosis: current pathogenesis and therapeutic options
1Institute for Cardiovascular Prevention, Ludwig-Maximilians-University Munich, Munich, Germany. christian.weber@med.uni-muenchen.de
Insights
Coronary artery disease (CAD) involves lipid metabolism and inflammation. New research targets these pathways to complement lipid-lowering therapies for atherosclerosis.
Area of Science:
- Cardiovascular Medicine
- Immunology
- Molecular Biology
Background:
- Coronary artery disease (CAD) is a major global health issue, primarily caused by atherosclerosis.
- Atherosclerosis pathogenesis involves disrupted lipid metabolism and chronic arterial wall inflammation.
- Leukocyte trafficking, chemokines, and their receptors are key regulators of this disturbed equilibrium.
Purpose of the Study:
- To systematically review recent molecular mechanisms in lipid-related inflammation in atherosclerosis and CAD.
- To explore translational developments and clinical strategies targeting these pathways.
- To highlight novel therapeutic targets complementing existing lipid-lowering treatments.
Main Methods:
- Systematic literature review of molecular mechanisms.
- Analysis of genetic profiling studies in human CAD.
- Survey of translational research and clinical strategies.
Main Results:
- Discovery of new pro- and anti-inflammatory pathways linking lipid and inflammation biology.
- Identification of genetic variations influencing human CAD.
- Unveiling of diverse targetable mechanisms for atherosclerosis treatment.
Conclusions:
- Targeting lipid-related inflammation offers a promising strategy to complement lipid-lowering therapies for CAD.
- Understanding molecular mechanisms and immune responses is crucial for developing novel therapeutic interventions.
- Further research into these pathways can lead to improved clinical strategies for managing atherosclerosis and CAD.
Abstract:
Coronary artery disease (CAD) arising from atherosclerosis is a leading cause of death and morbidity worldwide. The underlying pathogenesis involves an imbalanced lipid metabolism and a maladaptive immune response entailing a chronic inflammation of the arterial wall. The disturbed equilibrium of lipid accumulation, immune responses and their clearance is shaped by leukocyte trafficking and homeostasis governed by chemokines and their receptors. New pro- and anti-inflammatory pathways linking lipid and inflammation biology have been discovered, and genetic profiling studies have unveiled variations involved in human CAD. The growing understanding of the inflammatory processes and mediators has uncovered an intriguing diversity of targetable mechanisms that can be exploited to complement lipid-lowering therapies. Here we aim to systematically survey recently identified molecular mechanisms, translational developments and clinical strategies for targeting lipid-related inflammation in atherosclerosis and CAD.
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