Plasma Proteomics of the Fontan Circulation Reveal Signatures of Oxidative Stress and Cell Death
Authors' conclusion
Proteins from circulating microvesicles from patients with hypoplastic left heart syndrome post-Fontan are mostly from the liver. While this pilot study is limited by its sample size and may not represent the broader Fontan population, the proteomic changes were associated with worsening heart failure and cyanosis, suggesting their potential utility as biomarkers.
Study context
- Population
- Patients with hypoplastic left heart syndrome post-Fontan and controlsper group
- Participants
- n=6/group patients
- Comparison
- Plasma microvesicle proteomics in Fontan patients versus controls
- Fontann = 6
- Controlsn = 6
- Outcome
- Age
Main finding
As reported in the abstract
Fontan
16.0±2.1
Controls
15.3±2.2
Further findings
NYHA class and Fontan-associated liver disease among Fontan patients
- Fontan patients in New York Heart Association class II
- 3 of 6
- Fontan patients in New York Heart Association III/IV
- 3 of 6
- Fontan patients with Fontan-associated liver disease
- 4 of 6
Dysregulated proteins in Fontan failure
- Proteins upregulated
- 72
- Proteins downregulated
- 187
- Upregulated proteins predicted cell death pathways (Solute carrier family 2, Angiotensinogen, CD14) and mitochondrial reactive oxygen species signaling (ATP5F1A, S100A8)
- Downregulated proteins predicted impaired cell survival (tyrosine-protein kinase, endothelial growth factors) and mitochondrial antioxidant enzymes (GPX1, PRDX5)
- Fold change >1.5 or ≤1.5, P <0.05
Correlation of protein expression with worsening New York Heart Association class, ventricular function and cyanosis
- C1QA
- r =0.91
- HSPD1
- r =0.81
- ATP5F1A
- r =0.75
- ANK1
- r =0.63
- ACTN1
- r =0.76
Original publication
Plasma Proteomics of the Fontan Circulation Reveal Signatures of Oxidative Stress and Cell Death. Circ Heart Fail. Published 16 April 2025. doi:10.
Summarised from the published abstract; every number is checked against it