ReviewFrontiers in immunology2026
Immune dysregulation in chronic diabetic wounds: therapeutic opportunities for healing reprogramming.
Review in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Diabetic foot ulcers (DFUs) represent a devastating complication of diabetes mellitus, affecting approximately 25% of diabetic patients and contributing significantly to morbidity, mortality, and healthcare costs worldwide. Chronic non-healing wounds in diabetes are characterized by persistent inflammation, impaired immune cell function, and dysregulated cellular responses. The nucleotide-binding oligomerization domain-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome has emerged as a critical mediator of chronic inflammation and wound chronicity in diabetes. This comprehensive review examines the molecular mechanisms linking NLRP3 inflammasome activation, macrophage polarization dynamics, and wound healing impairment in diabetic conditions. We discuss how hyperglycemia-induced oxidative stress, advanced glycation end-products (AGEs), and mitochondrial dysfunction converge to activate the NLRP3 inflammasome, leading to caspase-1 activation, interleukin-1
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