Plasma extracellular vesicle levels of complement component 7 (C7) were significantly elevated in advanced fibrosis, yielding an AUC of 0.83 for differentiating advanced from mild fibrosis.
Observational (n=70)
No
Plasma extracellular vesicles contain distinct protein signatures that correlate with histological and imaging markers of MASLD severity, suggesting potential as non-invasive biomarkers.
Effect estimate: AUC 0.83 (95% CI 0.72-0.93)
p-value: p=0.002
Metabolic dysfunction-associated steatotic liver disease (MASLD) is increasing in both prevalence and severity, highlighting the need for non-invasive biomarkers to assess disease activity. Extracellular vesicles (EVs), which carry molecular cargo from their cells of origin, hold promise as accessible biomarkers. We performed proteomic profiling of plasma-derived EVs from 70 patients with MASLD to identify protein signatures associated with key histological features (steatosis, metabolic dysfunction-associated steatohepatitis (MASH), and fibrosis). These proteins were subsequently correlated with magnetic resonance (MR)-based liver imaging. Plasma EV protein profile differed between mild (S1) and advanced steatosis (S3). H4C1, OIT3, and ANPEP were elevated in S3, while CCDC25 and KLHL41 were decreased (|log2 fold change| > 1, p < 0.05). KLHL41 had a weak-to-moderate correlation with proton density fat fraction (PDFF) (R = −0.34, p = 0.016). GP1BA was upregulated in MASH (log2 fold change = 1.13, p = 0.03) but showed weak correlation with cT1, an imaging parameter for steatohepatitis (R = 0.22, p = 0.173). In fibrosis, complement component 7 (C7) was elevated in advanced (≥F3) vs. mild fibrosis (
Li et al. (2025) conducted an observational in Metabolic dysfunction-associated steatotic liver disease (MASLD) (n=70). Plasma extracellular vesicle (EV) protein biomarkers vs. Mild disease stages was evaluated on Differentiating <F3 vs. ≥F3 fibrosis using complement component 7 (C7) (AUC 0.83, 95% CI 0.72-0.93, p=0.002). Plasma extracellular vesicle levels of complement component 7 (C7) were significantly elevated in advanced fibrosis, yielding an AUC of 0.83 for differentiating advanced from mild fibrosis.
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