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Additionally, NLRP3 inflammasome was identified as a pivotal element in the inflammatory cascade of UC, which is a multi-protein complex that activates caspase-1 to convert pro-inflammatory cytokines into their active forms, thereby leading to the perpetuation of mucosal inflammation [7, 8]

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Targeting this pathway at multiple nodesincluding arginine transport, proline synthesis, and polyamine metabolismmay offer promising therapeutic strategies to halt fibrotic progression

However, a significant proportion of patients are still refractory to pharmacological treatments, so the development of new drugs targeting the underlying mechanisms of UC is necessary to achieve optimal disease control