The development of molecular biology and other new biotechnologies helps us to recognize the wound healing and non-healing wound of skin in the past 30 years. This review mainly focuses on the molecular biology of many cytokines (including growth factors) and other molecular factors such as extracellular matrix (ECM) on wound healing. The molecular biology in cell movement such as epidermal cells in wound healing was also discussed. Moreover many common chronic wounds such as pressure ulcers, leg ulcers, diabetic foot wounds, venous stasis ulcers, etc. usually deteriorate into non-healing wounds. Therefore the molecular biology such as advanced glycation end products (AGEs) and other molecular factors in diabetes non-healing wounds were also reviewed.

Macrophages play a critical role in wound healing and can be activated to two distinctive phenotypes in vitro: classical macrophage activation (caM) and alternative macrophage activation (aaM). This study investigated whether the impaired cutaneous repair observed in streptozotocin-induced diabetic rats was associated with altered macrophage activation. Our results show that macrophage activation phenotypes could be observed in wound healing through double immunostaining. The caM macrophages appeared in the initial stage of wound healing, followed by aaM macrophages, which predominated in normal wounds. However, through examining markers associated with activation by immunoblotting and real-time polymerase chain reaction (PCR), diabetic wounds demonstrated insufficient caM in the early stage but excessive aaM in the later proliferative phase. Moreover, the macrophage activation markers were correlated with the instructive T helper cell type 1 (Th1)/Th2 cytokines in both groups. It was indicated that changed macrophage activation might contribute to impaired healing in diabetes wounds, and that strategies for reverting this abnormal activation could be useful for enhancing the wound healing process.

The human hypertrophic scar undergoes hyperplasia and regression during progression. This study aimed to investigate whether fibroblasts in scar tissue undergo biological changes during the formation and regression of human hypertrophic scar. Using 32 scar samples, we measured collagen production by Masson's staining and the expression levels of transforming growth factor (TGF)-β1 and vascular endothelial growth factor (VEGF) by immunohistochemistry. In addition, fibroblasts from scar tissue were isolated and cultured, and total RNA was extracted for measurement of TGF-β1, VEGF and collagen transcript levels by reverse transcription-polymerase chain reaction (RT-PCR). Masson's staining showed that the number of fibroblasts and microvessels increased gradually in early and proliferative scars but decreased in regressive scars. Immunohistochemistry revealed that the expression of TGF-β1 and VEGF increased in early scars, peaked in proliferative scars and decreased in regressive scars. Moreover, the expression of TGF-β1, VEGF, collagen I and collagen III mRNAs also increased in early and proliferative scars and decreased significantly in regressive scars. Dynamic changes in fibroblast biology correlated with the formation and progression of hypertrophic scar.

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