Lipids & metabolic liver disease
Low-density Lipoprotein Cholesterol (LDL-C) and Total Cholesterol (TC) Mediate the Risk of PNPLA3 Inhibition in Cardiovascular Diseases
Authors' conclusion
This study suggests that PNPLA3 inhibition increases the risk of major CVDs. Moreover, blood LDL-C and TC may mediate a significant proportion of the associations between PNPLA3 inhibition and coronary atherosclerosis, coronary heart disease, or myocardial infarction.
Study context
- Population
- Genetic variants near the PNPLA3 gene linked to liver fat percentage used as instruments for PNPLA3 inhibition
- Comparison
- Genetically predicted PNPLA3 inhibition and risk of 10 cardiovascular diseases (CVDs), with lipid traits as mediators
- Outcome
- Risk of 10 CVDs
Methodological detailspositive control analyses on liver diseases
- Positive control analyses on liver diseases
Main finding
As reported in the abstract
CVD risk with genetically predicted PNPLA3 inhibition
- Coronary atherosclerosis
- 1.14 (95% CI 1.06, 1.23)
- Coronary heart disease
- 1.14 (95% CI 1.08, 1.21)
- MI
- 1.16 (95% CI 1.08, 1.26)
- HF, suggestive
- 1.09 (95% CI 1.02, 1.17; P = .0143)
- AF, suggestive
- 1.17 (95% CI 1.00, 1.36; P = .0468)
Further findings
Mediation by blood LDL-C and TC
- Proportion mediated, coronary atherosclerosis
- ≈16% to 25%
- Proportion mediated, MI
- 16% to 30%
- Proportion mediated, coronary heart disease
- 14% to 22%
Original publication
LDL-C and TC Mediate the Risk of PNPLA3 Inhibition in Cardiovascular Diseases. J Clin Endocrinol Metab. Published 18 April 2024. doi:10.
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