01

Disruption:

macrophages in diabetic wounds maintain a persistent inflammatory phenotype

linked to a failure in the interferon (IFN) β-Janus kinase (JAK)/signal transducer and activator of transcription 1 (STAT1) pathway, which normally regulates Setdb2 expression in wound macrophages.

01

elevated levels of pro-inflammatory cytokines such as IL-1β, TNF-α, IL-12, and IL-6, and an increased recruitment of inflammatory -macrophages.

02

affects the regulation of xanthine oxidase (XO)

leading to elevated uric acid (UA) levels in diabetic tissue

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• High UA levels exacerbate inflammation by increasing NF-κB-dependent transcription and activating the NLRP3 inflammasome, resulting in excessive IL-1β production.
• This dysregulation propagates a state of chronic inflammation that undermines normal wound healing in diabetes.

While these mechanisms highlight key contributors to the inflammatory environment in diabetic wounds, the precise regulation of UA and its role in sustaining this pathological state require further investigation.