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Radiation dermatitis (RD) remains a prevalent and challenging adverse effect of radiotherapy in cancer patients, significantly impairing patient quality of life and potentially interrupting treatment regimens. In recent years, the development of biopolymer-based hydrogels has emerged as a promising strategy for preventing and managing RD. Among these, alginate and chitosan-based hydrogels have attracted considerable attention due to their excellent biocompatibility, biodegradability, and wound-healing properties. This comprehensive review highlights the therapeutic efficacy of alginate/chitosan composite hydrogels in RD management. The unique physicochemical characteristics of these hydrogels, including moisture retention, oxygen permeability, and controlled drug release capabilities, make them ideal candidates for treating radiation-induced skin injuries. Mechanistically, these hydrogels exert anti-inflammatory, antioxidant, and antimicrobial effects while promoting re-epithelialization and collagen, which are critical in skin repair. Preclinical studies revealed significantly reduced RD severity scores and histopathological improvements following hydrogel application. Although clinical translation remains limited, initial trials showed promising outcomes in human subjects. Overall, alginate/chitosan hydrogels represent an effective system with immense potential to revolutionize RD management in oncological care.
Negative-pressure wound therapy (NPWT) is widely used in clinical practise to enhance wound healing; however, its biological effects on intact skin remain poorly understood. Given the expanding applications of NPWT, understanding its impact beyond open wounds is increasingly important. This study aimed to evaluate the biological responses of intact skin to negative-pressure, specifically focusing on epithelial-mesenchymal transition (EMT). The effects of negative-pressure loading were assessed using an in vitro model of non-diabetic human keratinocytes and an in vivo model of intact diabetic mouse skin. Human keratinocytes exposed to negative-pressure exhibited increased expression of thrombospondin-1 (THBS1), transforming growth factor-beta 1 (TGF-β1), plasminogen activator inhibitor-1 (PAI-1), and hypoxia-inducible factor 1-alpha (HIF-1α), alongside decreased epithelial markers and increased mesenchymal markers. These EMT-related changes were mitigated by inhibiting the THBS1-TGF-β1 interaction. Similarly, in diabetic mice, intermittent negative-pressure loading applied to intact dorsal skin significantly increased THBS1 and TGF-β1 levels, resulting in epidermal and dermal thickening, and promoted hypoxic, prothrombotic and angiogenic responses, as evidenced by increased HIF-1α, PAI-1, fibrinogen and vascular endothelial growth factor expression. These findings suggest that negative-pressure loading can induce EMT-like responses and tissue remodelling in intact skin primarily via mechanisms involving the THBS1-TGF-β1 signalling axis. This study expands the understanding of the biological influence of NPWT beyond traditional wound treatment applications, potentially informing future therapeutic considerations and safety guidelines.
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