Interleukin-10 Mitigates Chondrocyte Ferroptosis Associated With Haemophilic Arthropathy via Modulation of the STAT3 Signalling Pathway.

INTRODUCTION

Haemophilic arthropathy (HA) is characterized by recurrent intra-articular bleeding leading to cartilage degeneration. Ferroptosis plays a critical role in this process. While IL-10 is known to inhibit apoptosis, its effect on ferroptosis remains unexplored.

AIM: To investigate IL-10's role in chondrocyte ferroptosis in homophilic arthropathy via STAT3 signalling.

METHODS

Cartilage samples from HA and OA patients were analyzed by TEM and Western blot for iron deposition and IL-10. ATDC5 chondrocytes were treated with FAC (iron overload), Erastin (ferroptosis inducer) and IL-10±STAT3 inhibitor (AG-490). Cell viability assays, Western blotting, reactive oxygen species detection and immunofluorescent staining were performed. Viability, ROS and pathway proteins were assessed.

RESULTS

HA chondrocytes exhibited elevated mitochondrial iron deposition and reduced IL-10 versus OA controls. IL-10 suppressed ferroptosis with efficacy comparable to Fer-1, mechanistically dependent on STAT3 activation.

CONCLUSION

IL-10 suppresses ferroptosis in HA chondrocytes primarily via STAT3 signalling, providing theoretical support for its therapeutic potential for HA.