Table 1.

Main findings of relevant articles.

Year	Authors	Sample size	Main findings
2003	Peppa, M	100	• High AGE-containing diets increased skin AGE deposits, which decreased epithelialisation, angiogenesis, inflammation, granulation tissue deposition and collagen organisation up to 21 days, increased contraction and delayed wound closure
2004	Maggitti, KW	15	• Interaction of AGEs with the receptor for AGEs (RAGE) resulted in an exaggerated inflammatory response and compromised collagen production, which lead to impaired wound healing • sRAGE treated wounds show increased granulation tissue area and microvascular density
2005	Yavus, D	16	• Aminoguanidine improves wound healing, restores growth factor TGFbeta1 expression and preserves collagen ultrastructure, whereas it has no prominent effect on NO levels within wound tissue in diabetic rats
2008	Niu, YW	18	• Glycosylated matrix induced cell cycle arrest and apoptosis of cultured dermal fibroblasts, whereas application of RAGE-blocking antibodies redressed these changes
2009	Loughlin, DT	*	• Fibroblast/matrix interactions are altered as AGEs accumulate and affect focal adhesion formation • 3DG (3-deoxyglucosone) may be a factor mediating chronic wounds observed in patients with diabetes and in the elderly by altering the signalling within the fibroblast and inducing the missfolding of proteins
2011	Yuanchang, Z	50	• The plasma level of high mobility group box 1 (HMGB1) and its mRNA in white blood cells were found to be significantly higher in the wounded mice fed with high dietary AGEs than others
2012	Chen, SA	135	• The mixture of AuNP+EGCG+ALA (AuEA) significantly reduced the AGE-induced RAGE protein expression in fibroblasts (Hs68)
2012	Niu, YW	33	• Accumulation of AGEs in diabetic skin tissue induces an oxidative damage of fibroblasts and acts as an important contributor to the thinner diabetic abdominal dermis, demonstrated histologically by reduced thickness with shortened, thinned and disorganised collagen fibrils with focal chronic inflammatory cell infiltration
2012	Zhang, Q	14	• In vivo treatment with ethyl pyruvate (EP) significantly decreased wound HMGB1 levels (P <0.05), which was paralleled by increased wound breaking strength (P <0.05) and wound collagen content (P <0.05) • In vitro treatment with HMGB1 (100 ng/mL) had no effect on fibroblast proliferation but significantly reduced collagen synthesis (P <0.05). This effect was abrogated by co-treatment with anti-RAGE antibody • Fibroblasts treated with AGE had lower collagen synthesis (P <0.01), which was restored by anti-RAGE antibody treatment
2014	Pepe, D	16	• Gal-3, a matricellular protein upregulated in excisional skin repair and modulator of the inflammatory phase of repair and recently shown to be a receptor for AGEs (RAGE), decreases the accumulation of AGEs in wound healing
2014	Kim, S	70	• Tβ4r downregulated the receptor of AGE (RAGE) during the wound healing period • After treatment, Tβ4 improved wound healing markers such as wound closure, granulation and vascularisation (Tβ4 = Thymosin β4)
2016	Tian, M	36	• Deposition of AGE in diabetic rat skin activates the neutrophils even before injury. After injury, the normal physiological inflammatory reaction failed to occur adequately because exposure to AGE inhibited the viability of PMNs, promoted RAGE production and cell apoptosis, and prevented the migration of PMNs
2016	Das, A	10	• Hyperglycaemia and exposure to advanced glycated end products inactivated MFG-E8, impairing efferocytosis accompanied with persistent inflammation and slow wound closure • Topical recombinant MFG-E8 induced resolution of wound inflammation, improvements in angiogenesis and acceleration of closure

^*These studies represent histological studies with unspecified amounts of certain media.