DFU pathophysiology (”why healing stalls”)
Hyperglycemia → endothelial dysfunction & low NO, poor microperfusion.
Prolonged inflammation (M1-skewed macrophages), excess proteases, senescent cells.
ECM deficit + biofilm burden → weak keratinocyte/fibroblast migration and slow re-epithelialization.
How acellular fish-skin grafts (AFSGs) address this❓️
ECM mimic: Decellularized dermal collagen + natural porosity → a scaffold for keratinocyte/fibroblast migration, granulation, and capillary in-growth.
Omega-3–rich lipids: Provide precursors to specialized pro-resolving mediators (resolvins/protectins) that help tamp down chronic inflammation and support a shift toward pro-repair (M2) macrophage activity.
Moisture & barrier: Retains hydration, protects from protease-rich exudate, and can reduce dressing trauma/pain.
Adherence & handling: Conforms to irregular DFU beds, often reducing dressing-change frequency while maintaining a favorable microenvironment.
Takeaway: In a wound stuck in the inflammatory, ischemic, ECM-poor state, AFSGs supply a bioactive scaffold + lipid cues that help the ulcer transition back to orderly repair—as an adjunct to gold-standard care (debridement, off-loading, infection/perfusion/glycemic control).
Promising early data, but well-designed, multicenter RCTs are needed to confirm efficacy and ensure external validity
Reference
Zhao Y, Shen QQ. Acellular fish skin grafts in diabetic foot ulcer care: Advances and clinical insights. World J Diabetes. 2025 Jan 15;16(1):100597. doi: 10.4239/wjd.v16.i1.100597. PMID: 39817225; PMCID: PMC11718459.Activate to view larger image,
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