Identification of Iron Overload-Associated Biomarkers in the Synovium of Haemophilic Arthropathy

Haemophilic arthropathy (HA) is a common complication of haemophilia, characterized by progressive joint degeneration due to recurrent bleeding. Iron overload from erythrocyte lysis is thought to play a key role in HA pathogenesis, but its molecular basis remains unclear.

We performed data-independent acquisition (DIA) proteomics on synovial tissues from HA, osteoarthritis (OA) and rheumatoid arthritis (RA) patients. Bioinformatics analyses (GO, KEGG, PPI) were used to identify iron-related differentially expressed proteins (DEPs), and selected candidates were validated by Western blot.

Compared to OA and RA, HA synovium exhibited distinct expression patterns enriched in iron metabolism-related pathways, including ferroptosis and porphyrin metabolism. Key DEP such as FTH1 was upregulated, while SLC39A14 was downregulated. PPI analysis highlighted hub proteins involved in iron homeostasis.

This study identifies a unique iron overload-related proteomic signature in HA synovium, suggesting the potential biomarkers in disease progression. These findings provide novel molecular insights and potential targets for early HA intervention.