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One of the principal mechanisms involves hyperglycemia-induced oxidative stress and the consequent formation of advanced glycation end products (AGEs), which in turn activate two key inflammatory cascades: the Toll-like receptor (TLR) 2/4–MyD88–NF-κB pathway and the thioredoxin-interacting protein–NOD-like receptor pyrin domain-containing 3 (NLRP3) inflammasome complex (27–29)
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By targeting specific cellular pathways involved in tissue regeneration, these peptides hold the theoretical potential to accelerate healing and improve overall outcomes following surgical intervention
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