Healing after mammalian skin injury involves the interaction between numerous cellular constituents and regulatory factors, which together form three overlapping phases: an inflammatory response, a proliferation phase and a remodelling phase. Any slight variation in these three stages can substantially alter the healing process and resultant production of scars. Of particular significance are the mechanisms responsible for the scar‐free phenomenon observed in the foetus. Uncovering such mechanisms would offer great expectations in the treatment of scars and therefore represents an important area of investigation. In this review, we provide a comprehensive summary of studies on injury‐induced skin regeneration within the foetus. The information contained in these studies provides an opportunity for new insights into the treatment of clinical scars based on the cellular and molecular processes involved.

Key Points An integrated proteomics and metabolomics were used to investigate the pathogenesis of CRSwNP. Amino acid metabolism and mitochondrial dysfunction play key roles in the pathogenesis of CRSwNP.

Atopic dermatitis (AD) is a common, chronic inflammatory dermatosis with relapsing eruptions. Our study used bioinformatics to find novel candidate differentially expressed genes (DEGs) and predicted miRNAs between AD patients and healthy controls. The Mesh term “atopic dermatitis” was retrieved to obtain DEGs in GEO datasets. DEGs between AD patients and healthy controls were analyzed using GEO2R. Overlapping DEGs between different datasets were obtained with use of Draw Venn software. GO and KEGG enrichment analyses were conducted by the use of DAVID. STRING and miRWalk were used to individually analyze PPI networks, interactions of candidate genes and predicted miRNAs. A total of 571 skin samples, as retrieved from 9 databases were assessed. There were 225 overlapping DEGs between lesioned skin samples of AD patients and that of healthy controls. Nineteen nodes and 160 edges were found in the largest PPI cluster, consisting of 17 up-regulated and 2 down-regulated nodes. Two KEGG pathways were identified, including the cell cycle (CCNB1, CHEK1, BUB1B, MCM5) and p53 (CCNB1, CHEK1, GTSE1) pathways. There were 56 nodes and 100 edges obtained in the miRNA-target gene network, with has-miR-17-5p targeted to 4 genes and has-miR-106b-5p targeted to 3 genes. While these findings will require further verification as achieved with experiments involving in vivo and in vitro modles, these results provided some initial insights into dysfunctional inflammatory and immune responses associated with AD. Such information offers the potential to develop novel therapeutic targets for use in preventing and treating AD.