If a diabetic patient experiences poor wound healing, which mechanism explains why advanced glycation end-products (AGEs) impair fibroblast function in the extracellular matrix?

💡 Explanation

Poor wound healing in diabetes is linked to AGEs modifying collagen, thus impairing fibroblast function. Reduced collagen crosslinking and remodeling results because AGEs disrupt normal matrix interactions, therefore compromising tissue repair, rather than enhancing phagocytosis or angiogenesis.

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