MicroRNA-21 (miR-21), one of the early mammalian miRNAs identified, has been detected to be upregulated in multiple biological processes. Increasing evidence has demonstrated the potential values of miR-21 in cutaneous damage and skin wound healing, but lack of a review article to summarize the current evidence on this issue. Based on this review, relevant studies demonstrated that miR-21 played an essential role in wound healing by constituting a complex network with its targeted genes (i.e., PTEN, RECK. SPRY1/2, NF-κB, and TIMP3) and the cascaded signaling pathways (i.e., MAPK/ERK, PI3K/Akt, Wnt/β-catenin/MMP-7, and TGF-β/Smad7-Smad2/3). The treatment effectiveness developed by miR-21 might be associated with the promotion of the fibroblast differentiation, the improvement of angiogenesis, anti-inflammatory, enhancement of the collagen synthesis, and the re-epithelialization of the wound. Currently, miRNA nanocarrier systems have been developed, supporting the feasibility clinical feasibility of such miR-21-based therapy. After further investigations, miR-21 may serve as a potential therapeutic target for wound healing.

To evaluate cell morphology, crystal adhesion, cell damage, Calcium sensitive receptor (CaSR), and Claudin protein-14 (Claudin-14) expression at different time intervals and explore the role of nanobacteria in the formation of urinary calculi. In this experiment, HK-2 cells were cocultured with nanobacteria (NB) in the absence or presence of tetracycline (Tet). Cells treated with calcium oxalate monohydrate (COM) crystals were used as a positive control of urinary stone-induced cell damage. After which, cell morphology was evaluated by hematoxylin-eosin staining in comparison to untreated HK-2 cells (negative control). Use different methods to assess cell damage, crystal adhesion, and protein expression. (The degree of cell damage, crystal adhesion, and protein expression were evaluated by various methods). It was found that the degree of cell damage observed in Tet + NB-treated cells was significantly lower than that in NB-treated cells. Lactate dehydrogenase (LDH) leakage was higher in COM-exposed than in control cells ( P < 0.05 ). However, LDH release from both NB- and Tet + NB-treated cells was significantly lower than from COM-treated cells ( P < 0.05 ). The relative expression of CaSR and Claudin-14 proteins was higher in NB, COM, and TET + NB cells than in control cells ( P < 0.001 ) and was lower in Tet + NB than in NB cells ( P < 0.01 ). And P < 0.05 means that the difference was statistically significant, and P < 0.001 means that there was a significant difference between the both things. From the cell morphology, the cell damage in the COM group was greater than that in the NB group, and the cell damage markers in the COM group and the NB group were elevated. NB caused damage to HK-2 cells by inducing lipid peroxidation, and the degree of damage was increased in processing time. The adhesion of HK-2 cells to COM crystals increased after injury and was proportional to the duration of NB coculture. NB upregulated the expression of CaSR and Claudin-14 in HK-2 cells.

Efficacious wound healing is still a major concern for global healthcare due to the unsatisfactory outcomes under the current treatments. Leptin, an adipocyte-derived hormone, mainly acts in the hypothalamus and plays crucial roles in various biological processes. Recently, an increasing number of researches have shown that leptin played an important role in the wound healing process. In this review, we presented a first attempt to capture the current knowledge on the association between leptin and wound healing. After a comprehensive review, the molecular mechanisms underlying leptin in wound healing were speculated to be correlated to the regulation of inflammation of the macrophage and lymphocytes, angiogenesis, re-epithelialization, proliferation, and differentiation of fibroblasts. The affected genes and the signal pathways were multiple. For example, leptin was reported to ameliorate wound healing by its anti-inflammatory action, which might be correlated to the activation STAT1 and STAT3 via p38 MAPK or JAK2. However, the understanding of the specific role in each process (e.g., inflammatory, proliferative, and maturation phase) of wound repair is not entirely clear, and further studies are still warranted in both macrostructural and microscale factors. Therefore, identifying and validating the biological mechanisms of leptin in wound healing is of great significance to develop potential therapeutic targets for the treatment of wound healing in clinical practice.

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