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Galectin-3 and peripheral artery disease: a Mendelian randomization study.

Yang Gou¹, Miao Chen¹, Zhi Zhu¹

¹Department of General Surgery, The Third People's Hospital of Chengdu, Chengdu, Sichuan Province, China.

Frontiers in Cardiovascular Medicine

|January 19, 2024

Summary

This study investigated if galectin-3 (Gal-3) levels causally influence peripheral arterial disease (PAD). Mendelian randomization analysis found no significant causal link between Gal-3 and PAD, suggesting current correlations may not indicate causation.

Keywords:

Mendelian randomization SNPs (single-nucleotide polymorphisms)causality galectin-3 peripheral artery disease

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Area of Science:

Cardiovascular Research
Genetics
Biomarkers

Background:

Elevated circulating galectin-3 (Gal-3) is correlated with peripheral arterial disease (PAD) diagnosis and severity.
The underlying causal relationship between Gal-3 and PAD remains unclear.

Purpose of the Study:

To evaluate the potential causal relationship between galectin-3 (Gal-3) levels and peripheral arterial disease (PAD) using Mendelian randomization.
To determine if genetic predisposition to higher Gal-3 levels increases PAD risk.

Main Methods:

Two-sample Mendelian randomization (MR) analysis was performed using genome-wide association study (GWAS) data.
Six single-nucleotide polymorphisms (SNPs) associated with Gal-3 served as instrumental variables.
MR-Egger, inverse variance weighted (IVW), weighted median, and weighted mode regression techniques were employed.

Main Results:

No statistically significant causal association was found between Gal-3 and PAD (IVW OR = 0.9869, P = 0.8232).
Genetic pleiotropy analysis indicated no significant impact on the putative causal relationship (MR-Egger intercept P = 0.659).

Conclusions:

Current evidence does not support a causal relationship between circulating galectin-3 levels and peripheral arterial disease.
The observed correlation between Gal-3 and PAD may not be directly causal.