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Fibrosis Process Activation in Patients with Acute Cardiac Rejection: A Novel Noninvasive Diagnostic Approach
Marta Delgado-Arija1,2, Lorena Pérez-Carrillo1,2, Irene González-Torrent1
1Clinical and Translational Research in Cardiology Unit, Health Research Institute Hospital La Fe (IIS La Fe), Avd. Fernando Abril Martorell 106, 46026 Valencia, Spain.
Biomedicines
|June 26, 2026
Summary
Altered serum mRNAs linked to cardiac fibrosis, including fibroblast activators and TGF-β/WNT pathways, were identified in heart transplant recipients with acute cellular rejection (ACR). Specific markers show high accuracy in detecting moderate to severe rejection.
Area of Science:
- Cardiology
- Immunology
- Molecular Biology
Background:
- Cardiac allograft fibrosis limits long-term graft survival after heart transplantation.
- The fibrotic process during acute cellular rejection (ACR) in cardiac allografts is not well understood.
Purpose of the Study:
- To identify serum messenger RNAs (mRNAs) associated with cardiac fibrosis in ACR patients.
- To assess the diagnostic accuracy of these mRNAs for detecting rejection episodes.
Main Methods:
- Analysis of 40 serum samples from heart transplant recipients undergoing routine endomyocardial biopsies.
- Comparison of serum mRNA profiles between patients with ACR (grades ≥ 1R) and those without rejection.
Main Results:
- Several fibrosis-related mRNAs were altered in ACR patients.
- Significant differences in fibroblast/myofibroblast activators (TNS1, FAP, ACTA2) and TGF-β/WNT signaling pathways (TGFBR1, JAK1, WNT7A, WLS) were observed.
- TNS1 and WLS demonstrated high diagnostic accuracy (AUC > 0.90) for moderate to severe cardiac rejection.
Conclusions:
- Circulating fibroblast activators (FAP, ACTA2) and profibrotic pathways (TGF-β, WNT) are altered in clinically relevant cardiac rejection.
- These findings may enhance surveillance strategies for heart transplant patients.
- Potential for new therapeutic targets to inhibit fibrosis activation in cardiac allografts.
