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Published on: February 20, 2019
LRG1 as a Potential Therapeutic Target in Atherosclerosis: Mechanistic Basis and Current Evidence
Jianan Wu1, Xia Yi1, Lanlan Wang1
1College of Acupuncture-Moxibustion, Tuina and Rehabilitation, Hunan University of Chinese Medicine, Changsha 410208, China.
Insights
Leucine-rich α-2-glycoprotein 1 (LRG1) shows potential as a therapeutic target for atherosclerosis (AS). This review explores LRG1
Area of Science:
- Cardiovascular Biology
- Inflammation
- Molecular Medicine
Background:
- Atherosclerosis (AS) is a chronic inflammatory arterial disease underlying major cardiovascular disorders.
- Existing therapies reduce but do not eliminate residual cardiovascular risk, necessitating novel molecular targets.
- Leucine-rich α-2-glycoprotein 1 (LRG1), an inflammation-inducible glycoprotein, is implicated in vascular pathologies.
Purpose of the Study:
- To review the biological characteristics of LRG1.
- To examine the evidence linking LRG1 to atherosclerosis.
- To discuss LRG1's potential mechanisms, therapeutic feasibility, and limitations in AS.
Main Methods:
- Literature review of studies on LRG1 and atherosclerosis.
- Analysis of LRG1's role in macrophage polarization, endothelial function, angiogenesis, and extracellular matrix remodeling.
- Examination of clinical associations, plaque localization, and experimental models.
Main Results:
- LRG1 is associated with AS clinically and experimentally.
- LRG1 may promote pro-inflammatory macrophage polarization and disturb endothelial homeostasis.
- LRG1 influences angiogenesis and extracellular matrix remodeling, contributing to plaque changes.
Conclusions:
- LRG1 is implicated in multiple pathogenic aspects of atherosclerosis.
- LRG1 presents a promising, though not fully validated, therapeutic target for AS.
- Further research is needed to fully elucidate LRG1's role and therapeutic potential in AS.
Abstract:
Atherosclerosis (AS) is a chronic inflammatory disease of large arteries. It underlies many cardiovascular disorders, including coronary artery disease, myocardial infarction, stroke, and peripheral arterial disease. Current therapies have improved outcomes, especially lipid-lowering, antithrombotic, and anti-inflammatory treatments. Yet residual cardiovascular risk remains, and new molecular targets are still needed. Leucine-rich α-2-glycoprotein 1 (LRG1) is an inflammation-inducible secreted glycoprotein. It has drawn attention because it is linked to pathological angiogenesis, vascular dysfunction, tissue remodeling, and fibrosis. Recent studies indicate that LRG1 is related to AS at several levels. These include circulating clinical associations, plaque localization, and experimental models. In AS, LRG1 may not simply act as a biomarker. It may promote macrophage pro-inflammatory polarization, disturb endothelial homeostasis, support abnormal angiogenesis, and influence extracellular matrix remodeling and plaque structural change. This review examines the biological features of LRG1 and the current evidence connecting it with AS. It also discusses possible mechanisms, therapeutic feasibility, and current limitations. Overall, LRG1 appears to be a promising but still incompletely validated candidate target in AS.
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