Lipids & metabolic liver disease
Proteomic signature of metabolic dysfunction-associated steatotic liver disease and risk of atherosclerotic cardiovascular disease
Authors' conclusion
This suggests that cProMASLD may capture MASLD-related physiological heterogeneity beyond clinical MASLD classification.
Study context
- Population
- UK Biobank participants; 35.26% with MASLD at baseline6,014 developed atherosclerotic cardiovascular disease (ASCVD)
- Participants
- 40,913 participants
- Exposure
- Clinical MASLD and proteomics-inferred MASLD and risk of ASCVD subtypes
- MASLDn = 14,425
- Outcome
- Incident ASCVD subtypes: IHD, PAD and stroke
- Follow-up
- Median 13.42 years [IQR, 12.52-14.22]
Methodological detailsUK Biobank, two-step Mendelian randomization, prediction model development (Pro-SCORE2)
- UK Biobank
- Two-step Mendelian randomization
- Prediction model development (Pro-SCORE2)
Main finding
As reported in the abstract
Risk of ASCVD subtypes
Hazard ratio (95% CI)
MASLDIHD
1.50(1.41–1.60)
cProMASLDIHD
1.58(1.48–1.68)
MASLDPAD
1.25(1.09–1.44)
cProMASLDPAD
1.43(1.24–1.64)
MASLDstroke
1.19(1.08–1.31)
cProMASLDstroke
1.21(1.10–1.34)
Observational data: associations, not effects.
Further findings
cProMASLD and ASCVD risk adjusted for MASLD
- cProMASLD remained positively associated with ASCVD risk after adjusting for MASLD
Proteins mediating MASLD–ASCVD subtype associations
- Mediating proteins, MASLD-IHD
- 15
- Mediating proteins, MASLD-PAD
- 3
- Mediating proteins, MASLD-stroke
- 3
- FABP4 mediation proportion (MASLD-IHD)
- 15.12%
- IL7R mediation proportion (MASLD-PAD)
- 7.45%
- EDA2R mediation proportion (MASLD-stroke)
- 9.24%
- Two-step Mendelian randomization
ASCVD risk prediction in MASLD population, Pro-SCORE2 vs SCORE2
- C-index increase
- 7.5-9.6%
- 10-year AUC increase
- 5.8-9.2%
Original publication
Proteomic signature of metabolic dysfunction-associated steatotic liver disease and risk of atherosclerotic cardiovascular disease. Cardiovasc Diabetol. Published 14 December 2025. doi:10.
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