What you carry at this position in your DNA and what research says about it.
Cardiovascular Risk: 10/10 evidence, 23 publications.
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Sample genotype (not yours): A/A
Typical Cardiovascular and Vessel Risk
Inheriting two copies of the reference allele is associated with lower circulating suPAR levels. This helps maintain typical blood vessel integrity and a baseline risk for cardiovascular events.
What this genotype means: Lower circulating suPAR levels; Typical risk of abdominal aortic aneurysm; Higher baseline HDL cholesterol.
Sample genotype (not yours): A/G
Slightly Increased Cardiovascular and Vessel Risk
Carrying one copy of the G allele leads to moderately elevated suPAR levels in the blood. This moderate increase is linked to a slightly higher risk of vascular inflammation and arterial plaque buildup.
What this genotype means: Moderately elevated suPAR levels; Slightly higher risk of abdominal aortic aneurysm; Slightly lower HDL cholesterol.
Sample genotype (not yours): G/G
Elevated Cardiovascular and Vessel Risk
Inheriting two copies of the G allele results in significantly higher circulating suPAR levels. This elevation is strongly linked to increased vascular inflammation, arterial plaque formation, and vessel wall weakness.
What this genotype means: Significantly elevated suPAR levels; Higher risk of abdominal aortic aneurysm; Lowest baseline HDL cholesterol.
Gene function and biological role
Gene Function: The PLAUR gene encodes the urokinase plasminogen activator receptor, a cell-surface protein that plays a central role in regulating tissue remodeling, cell migration, and localized blood clotting. Under conditions of inflammation or tissue injury, this receptor is cleaved and released into the bloodstream as a soluble form known as suPAR [1]. Circulating suPAR acts as an active signaling molecule that modulates immune cell behavior and promotes inflammatory processes within blood vessel walls [2]. Elevated levels of suPAR are widely recognized as a strong biomarker and causal driver of systemic vascular inflammation, accelerated atherosclerosis, and progressive kidney damage [2].
Variant Impact: The rs4760 variant is a missense mutation in the PLAUR gene that alters the amino acid at position 317 from leucine to proline. This structural modification in the C-terminal region of the receptor significantly increases the shedding and cleavage of the receptor from cell membranes [1]. Consequently, the variant allele leads to a dramatic elevation of circulating suPAR levels in the bloodstream [1]. This increase in suPAR promotes a pro-inflammatory state in monocytes, accelerating plaque formation in the arteries and weakening vascular walls [3].
Key Insight: The rs4760 variant is one of the strongest genetic regulators of suPAR, a protein that directly drives both cardiovascular plaque buildup and chronic kidney disease.
Location: PLAUR. Chromosome 19 · 19q13.31 · 43.6 Mb
Estimated prevalence by population
Global 80.0%; European 70.9%; African 95.1%; East Asian 99.5%; South Asian 75.2%; Americas 82.1%; Ashkenazi 84.9%; Finnish 67.7%; Middle Eastern 85.6%; Amish 66.9%.
Estimated AA genotype frequency.
Global 18.5%; European 26.6%; African 4.9%; East Asian 0.5%; South Asian 23.1%; Americas 17.0%; Ashkenazi 14.5%; Finnish 29.2%; Middle Eastern 13.8%; Amish 29.8%.
Estimated AG genotype frequency.
Global 1.5%; European 2.5%; African 0.1%; East Asian < 0.1%; South Asian 1.8%; Americas 0.9%; Ashkenazi 0.6%; Finnish 3.1%; Middle Eastern 0.6%; Amish 3.3%.
Estimated GG genotype frequency.
Showing effects for A/A genotype
Cardiovascular & Metabolic
Vascular Health & Aneurysm
Aortic Aneurysm. Evidence: 10/10. Source: PMID 37845353. Typical Risk.
Lipids & Cholesterol
HDL Cholesterol. Evidence: 10/10. Source: PMID 32203549. Higher HDL.
Blood Cell & Iron Traits
Neutrophil Count. Evidence: 10/10. Source: PMID 27863252. Higher Count.
Basophil Count. Evidence: 10/10. Source: PMID 27863252. Higher Count.
Immature Granulocytes. Evidence: 6/10. Source: PMID 37596262. Higher Count.
Immunity & Inflammation
Inflammatory & Circulating Protein Markers
Endoglin Levels. Evidence: 10/10. Source: PMID 34648354. Typical Level.
Showing effects for A/G genotype
Aortic Aneurysm. Evidence: 10/10. Source: PMID 37845353. Increased Risk.
HDL Cholesterol. Evidence: 10/10. Source: PMID 32203549. Slightly Lower HDL.
Neutrophil Count. Evidence: 10/10. Source: PMID 27863252. Slightly Lower.
Basophil Count. Evidence: 10/10. Source: PMID 27863252. Slightly Lower.
Immature Granulocytes. Evidence: 6/10. Source: PMID 37596262. Slightly Lower.
Endoglin Levels. Evidence: 10/10. Source: PMID 34648354. Slightly Elevated.
Showing effects for G/G genotype
Aortic Aneurysm. Evidence: 10/10. Source: PMID 37845353. Highest Risk.
HDL Cholesterol. Evidence: 10/10. Source: PMID 32203549. Lowest HDL.
Neutrophil Count. Evidence: 10/10. Source: PMID 27863252. Lowest Count.
Basophil Count. Evidence: 10/10. Source: PMID 27863252. Lowest Count.
Immature Granulocytes. Evidence: 6/10. Source: PMID 37596262. Lowest Count.
Endoglin Levels. Evidence: 10/10. Source: PMID 34648354. Highest Level.
What this genotype means for the people who carry it
Sample genotype: AA (Homozygous)
Maintaining lower levels of the inflammatory marker suPAR is highly protective for the vascular system [1]. Cellular studies show that the reference leucine residue at position 317 keeps the urokinase receptor securely anchored to cell membranes, preventing excessive shedding into the bloodstream [1]. Consequently, there is less systemic vascular inflammation and a lower rate of arterial plaque accumulation [1]. Large-scale genetic cohorts confirm that this baseline state correlates with a typical risk of developing abdominal aortic aneurysms [2]. Additionally, this genotype is associated with higher levels of protective HDL cholesterol, which further supports overall heart health [3]. Immune profiles show slightly higher baseline neutrophil and basophil counts, representing typical immune surveillance patterns [4].
Lower circulating suPAR levels; Typical risk of abdominal aortic aneurysm; Higher baseline HDL cholesterol.
Sample genotype: AG (Heterozygous)
Possessing a single copy of the proline-encoding G allele alters the physical structure of the urokinase receptor, making it more susceptible to enzymatic cleavage [1]. This structural change results in a moderate increase in circulating suPAR levels, which can trigger low-grade vascular inflammation [1]. Over time, elevated suPAR levels encourage circulating monocytes to adhere to blood vessel walls, accelerating the early stages of atherosclerosis [1]. Clinical data link this moderate elevation to a slightly increased risk of developing abdominal aortic aneurysms [2]. Lipid profiles also show a minor reduction in protective HDL cholesterol levels, which can subtly influence overall cardiovascular health [3]. Slight shifts in white blood cell populations, including minor decreases in neutrophil and basophil counts, are also observed [4].
Moderately elevated suPAR levels; Slightly higher risk of abdominal aortic aneurysm; Slightly lower HDL cholesterol.
Sample genotype: GG (Homozygous)
Having two copies of the proline-encoding G allele causes maximum shedding of the urokinase receptor, leading to highly elevated levels of circulating suPAR [1]. High suPAR levels act as a strong inflammatory stimulus, driving monocytes to infiltrate arterial walls and accelerate plaque formation [1]. This chronic inflammatory state weakens the structural integrity of major blood vessels, significantly increasing the risk of abdominal aortic aneurysms [2]. Large-scale genetic studies consistently link this genotype to a higher incidence of atherosclerotic cardiovascular events [2]. Furthermore, individuals with this genotype tend to have the lowest levels of protective HDL cholesterol, compounding their cardiovascular risk profile [3]. Marked shifts in immune cell counts are also present, characterized by lower baseline levels of neutrophils and basophils [4].
Significantly elevated suPAR levels; Higher risk of abdominal aortic aneurysm; Lowest baseline HDL cholesterol.
Variants with shared genetic architecture
rs6841581 · EDNRA Gene · Chr 4 · Heart Disease Risk
rs7500448 · CDH13 Gene · Chr 16 · Heart Disease Risk
rs3825807 · ADAMTS7 Gene · Chr 15 · Coronary Artery Disease Risk
The Polygenic and Monogenic Basis of Blood Traits and Diseases.
Diversity and scale: Genetic architecture of 2068 traits in the VA Million Veteran Program.
A cross-population atlas of genetic associations for 220 human phenotypes.
The Allelic Landscape of Human Blood Cell Trait Variation and Links to Common Complex Disease.
Content updated August 2026.
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