In addition to its barrier function, the skin plays a crucial role in maintaining the stability of the body's internal environment and normal physiological functions. When the skin is damaged, it is important to select proper dressings as temporary barriers to cover the wound, which can exert significant effects on defence against microbial infection, maintaining normal tissue/cell functions, and coordinating the process of wound repair and regeneration. It now forms an important approach in clinic practice to facilitate wound repair. We conducted a comprehensive literature search using online databases including PubMed, Web of Science, MEDLINE, ScienceDirect, Wiley Online Library, CNKI, and Wanfang Data. In addition, information was obtained from local and foreign books on biomaterials science and traumatology. This review focuses on the efficacy and principles of functional dressings for anti-bacteria, anti-infection, anti-inflammation, anti-oxidation, hemostasis, and wound healing facilitation; and analyses the research progress of dressings carrying living cells such as fibroblasts, keratinocytes, skin appendage cells, and stem cells from different origins. We also summarize the recent advances in intelligent wound dressings with respect to real-time monitoring, automatic drug delivery, and precise adjustment according to the actual wound microenvironment. In addition, this review explores and compares the characteristics, advantages and disadvantages, mechanisms of actions, and application scopes of dressings made from different materials. The real-time and dynamic acquisition and analysis of wound conditions are crucial for wound management and prognostic evaluation. Therefore, the development of modern dressings that integrate multiple functions, have high similarity to the skin, and are highly intelligent will be the focus of future research, which could drive efficient wound management and personalized medicine, and ultimately facilitate the translation of health monitoring into clinical practice.

Although it is well-known that human skin aging is accompanied by an alteration in the skin microbiota, we know little about how the composition of these changes during the course of aging and the effects of age-related skin microbes on aging. Using 16S ribosomal DNA and internal transcribed spacer ribosomal DNA sequencing to profile the microbiomes of 160 skin samples from two anatomical sites, the cheek and the abdomen, on 80 individuals of varying ages, we developed age-related microbiota profiles for both intrinsic skin aging and photoaging to provide an improved understanding of the age-dependent variation in skin microbial composition. According to the landscape, the microbial composition in the Children group was significantly different from that in the other age groups. Further correlation analysis with clinical parameters and functional prediction in each group revealed that high enrichment of nine microbial communities (i.e., Cyanobacteria, Staphylococcus, Cutibacterium, Lactobacillus, Corynebacterium, Streptococcus, Neisseria, Candida, and Malassezia) and 18 pathways (such as biosynthesis of antibiotics) potentially affected skin aging, implying that skin microbiomes may perform key functions in skin aging by regulating the immune response, resistance to ultraviolet light, and biosynthesis and metabolism of age-related substances. Our work re-establishes that skin microbiomes play an important regulatory role in the aging process and opens a new approach for targeted microbial therapy for skin aging.

Normal wound repair is a dynamic and complex process involving multiple coordinated interactions between growth factors, cytokines, chemokines, and various cells. Any failure during the repair process may cause chronic wounds or scar formation, which increase the financial burden of patients due to repetitive treatments and considerable medical expenditures, and affect their quality of life. Nowadays, extensive efforts have been made to develop novel therapeutics for wound repair. Genetic engineering technology, tissue engineering technology, stem cell-based therapy, physical and biochemical technology, and vacuum-assisted closure technique have been proposed to be beneficial for wound repair, and shown considerable potential for improving the rate and quality of wound healing and skin regeneration. However, challenges remain as applying these techniques. As the development of cell biology and molecular biology, the understanding of the mechanism under wound repair has gradually deepened. As the growth of interdisciplinary research on physics, chemistry, biology, tissue engineering, and materials, the concept and technique relating wound repair for clinical application have rapidly developed. This article reviews the latest progress on the mechanism and technique in wound repair.

Keloids, partially considered as benign tumors, are characterized by the overgrowth of fibrosis beyond the boundaries of the wound and are regulated mainly by transforming growth factor (TGF)-β1, which induces the transition of fibroblasts to myofibroblasts. Hypoxia is an important driving force in the development of lung and liver fibrosis by activating hypoxia inducible factor-1α and stimulating epithelial‑mesenchymal transition. However, it is unknown whether and hypoxia can influence human dermal scarring. The aim of this study was to investigate whether hypoxia drives the transition of dermal fibroblasts to myofibroblasts and to clarify the potential transduction mechanisms involved. First, we observed that keloids are a relatively hypoxic tissue. Second, we found that hypoxia drives the transition of normal dermal fibroblasts to a myofibroblast-like phenotype [high expression of α-smooth muscle actin (α-SMA) and collagen I and III]. Finally, hypoxia effectively facilitated the nuclear import of the Smad2 and Smad3 complex, while blockade with the Smad3 inhibitor, SIS3, significantly impaired the expression of hypoxia-induced fibrosis-related molecules. Taken together, to the best of our knowledge, this study demonstrates for the first time that hypoxia facilitates the transition of dermal fibroblasts to myofibroblasts through the activation of the TGF-β1/Smad3 signaling pathway and our findings may provide a potential target for the treatment of keloids.