Serum and Urinary Proteomic Signatures Revealing Redox and Metabolic Dysregulation in Acute Achilles Tendon Rupture.

Objectives: The etiology of acute Achilles tendon rupture (ATR) remains elusive. A comprehensive case-control study of the proteome profile was conducted to gain insights into the potential pathogenesis of acute ATR and identify novel biomarkers.

Method: Serum and urine samples were collected from 15 acute ATR patients and 15 healthy individuals for proteome analysis. Protein levels were assessed using isobaric tags for relative and absolute quantitation (iTRAQ) for serum and label-free proteomic approaches for urine. Differential expression was considered significant at levels exceeding 2-fold (for urine) and 1.2-fold (for serum), with a p-value below 0.05.

Results: In serum and urine samples, 44 and 198 proteins were identified, respectively, which exhibit significant differences between acute ATRs and normal Achilles tendons. Our bioinformatics analysis revealed the involvement of multiple biological processes and pathways in acute ATRs, including immune response, metabolism, and redox regulatory pathways. Several differentially expressed proteins were found to participate in various metabolic pathways, suggesting their potential pivotal roles in ATR pathogenesis. Furthermore, protein-protein interaction analysis of the differentially expressed proteins (P<0.05) highlighted abnormalities in major protein-protein interaction hubs, specifically pyruvate kinase (PKM), peroxiredoxin-1 (PRDX1), phosphoglycerate kinase 1 (PKG1), profilin-1, and apolipoprotein A-IV, observed in the serum and urine samples of acute ATR patients.

Conclusion: Abnormal nitrogen, carbohydrate, glucose, and long-chain fatty acid metabolic proteins, as well as PKM, PRDX1, and PGK1 abnormalities, may be involved in the pathogenesis of acute ATR.