Proteomic signatures characterized by inflammatory signaling and metabolic processes have divergent associations with 30-year incidence of coronary artery disease in type 1 diabetes: the Pittsburgh Epidemiology of Diabetes Complications cohort
Authors' conclusion
In this prospective analysis of a type 1 diabetes cohort, a protein signature characterized by inflammatory signaling partially mediated the effect of hyperglycemia on hCAD, while a signature characterized by metabolic processes including lipid catabolism and hormone response was associated with hCAD protection independent of glycemia.
Study context
- Population
- Childhood-onset (< 17 years) T1D, Pittsburgh Epidemiology of Diabetes Complications cohort; baseline mean age 30, mean diabetes duration 22 years
- Participants
- 417 participants
- Exposure
- Protein modules and 30-year incident hard coronary artery disease (CAD)
- Outcome
- Incident hard CAD (hCAD; CAD death, nonfatal MI, revascularization, or blockage ≥ 50%)
- Follow-up
- 30-year
Methodological detailshigh-throughput proteomics, weighted correlation network analysis, causal mediation analysis
- High-throughput proteomics
- Weighted correlation network analysis
- Causal mediation analysis
Main finding
As reported in the abstract
Incident hard CAD (hCAD)
151 participants
36.2%
Proportion of total HbA1c effect on hCAD mediated by the inflammatory module
14%
Observational data: associations, not effects.
Further findings
Incident hCAD · 30-year
- Participants with incident hCAD
- 151 (36.2%)
Mediation of HbA1c effect on hCAD
- Proportion of total HbA1c effect on hCAD mediated by module 1
- 14%
Parts of this Brief are withheld: the automatic checks could not confirm them against the abstract.
Original publication
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