Hypertrophic scarring is the most serious and unmet challenge following burn and trauma injury and often leads to pain, itching and even loss of function. However, the demand for ideal scar prevention and treatment is difficult to satisfy. We aimed to discover the effects and mechanisms of adipose-derived stem cell (ADSC) exosomes in hypertrophic scarring. ADSC exosomes were isolated from the culture supernatant of ADSCs and identified by nanoparticle tracking analysis, transmission electron microscopy and western blotting. The effect of ADSC exosomes on wound healing and scar formation was detected by the wound model of BALB/c mice. We isolated myofibroblasts from hypertrophic scar tissue and detected the cell viability, proliferation and migration of myofibroblasts. In addition, collagen formation and fibrosis-related molecules were also detected. To further disclose the mechanism of ADSC exosomes on fibrosis in myofibroblasts, we detected the expression of Smad2 in hypertrophic scar tissue and normal skin and the regulatory mechanism of ADSC exosomes on Smad2. Injection of bleomycin was performed in male BALB/c mice to establish an in vivo fibrosis model while ADSC exosomes were administered to observe their protective effect. The tissue injury of mice was observed via hematoxylin and eosin and Masson staining and related testing. In this study, we found that ADSC exosomes could not only speed up wound healing and improve healing quality but also prevent scar formation. ADSC exosomes inhibited expression of fibrosis-related molecules such as α-smooth muscle actin, collagen I (COL1) and COL3 and inhibited the transdifferentiation of myofibroblasts. In addition, we verified that Smad2 is highly expressed in both hypertrophic scar tissue and hypertrophic fibroblasts, while ADSC exosomes downregulated the expression of Smad2 in hypertrophic fibroblasts. Further regulatory mechanism analysis revealed that microRNA-125b-5p (miR-125b-5p) is highly expressed in ADSC exosomes and binds to the 3′ untranslated region of Smad2, thus inhibiting its expression. In vivo experiments also revealed that ADSC exosomes could alleviate bleomycin-induced skin fibrosis and downregulate the expression of Smad2. We found that ADSC exosomes could alleviate hypertrophic scars via the suppression of Smad2 by the specific delivery of miR-125b-5p.

Human adipose-derived stromal cells (ADSCs) are receiving unprecedented attention as a potential cellular source for regenerative medicine-based therapies against various diseases and conditions. However, there still have significant issues concerning the translational development of ADSC-based therapies, such as its heterogeneity and being prone to aging. We developed a new simple and economical 3D semi-suspended expansion method in which 3D spheroids reside on an ADSC-derived self-feeder cell layer, producing cells with increased population homogeneity and strong stemness and ensuring that the proliferation and differentiation potency of the cells does not become notably reduced after at least ten passages in culture. To check the potential application of the 3D ADSC spheroids, we discovered that the combination of siEID3, which is a small interfering RNA of EP300 inhibitor of differentiation 3 (EID3), and laminin/poly-d-lysine matrix can rapidly result in trans-differentiation of the 3D spheroid cells to neural progenitor-like cells (NPLCs) in approximately 9 days in vitro. This approach provides a multidisciplinary tool for stem cell research and production in mesenchymal stem cell-related fields.

The incidence of androgenetic alopecia in males is on the rise annually, with hair transplantation using follicular unit extraction (FUE) gaining increasing acceptance as an appropriate treatment for these individuals. A retrospective study was undertaken, involving 158 male patients diagnosed with androgenetic alopecia, who underwent treatment between January 2016 and December 2020 at the Medical Cosmetology Department of the First Affiliated Hospital of Xi’an Medical University. Demographic data and treatment characteristics were documented and analyzed. Clinical efficacy, operation-related complications, patient satisfaction rates, and quality of life scores were assessed and analyzed. Following FUE hair transplantation, over 90% of the hair follicles survived in 158 patients, with more than 85% of patients achieving a hair follicle survival rate exceeding 95% at 12 months post-operation. Patient satisfaction rates exceeded 98%, while the complication rate was below 6%. Our findings demonstrate that FUE is a minimally invasive hair transplant technique associated with a high hair follicle survival rate and optimal hair density. This approach proves effective in treating male androgenetic alopecia and merits further clinical application.

Background: Diabetic foot ulcers (DFUs) represent a severe complication of diabetes, often leading to chronic non-healing wounds and high amputation risk. Lactylation, a recently recognized post-translational modification driven by lactate metabolism, has emerged as a key regulator of immune response and gene expression. However, its role in DFU pathogenesis remains largely unexplored. This study aims to systematically investigate lactylation-related genes and their association with immune dysregulation in DFUs. Methods: Transcriptomic data from three GEO datasets (GSE134431, GSE80178, GSE68183) were integrated and normalized to identify differentially expressed genes (DEGs). A lactylation-related gene set was compiled from published literature. Machine learning approaches, including LASSO regression and Random Forest, were applied to screen for core genes. Immune infiltration profiles were assessed using ssGSEA. Experimental validation was conducted in high-glucose-stimulated macrophages and human DFU tissues via qPCR, Western blot, immunohistochemistry, and immunofluorescence. Results: We integrated three transcriptomic datasets comprising 25 DFU and 14 normal tissues, identifying 1,234 differentially expressed genes (DEGs). Among these, 38 overlapped with lactylation-related genes, with 27 significantly downregulated in DFU. Machine learning algorithms identified three core lactylation-associated genes: CHD4, EEF1A1, and EEF1G, which exhibited significant downregulation in DFU and demonstrated high within cohort classification performance with AUC values of 0.860, 0.926, and 0.989, respectively. Immune infiltration analysis revealed these genes positively correlated with natural killer cells and negatively correlated with neutrophil infiltration. Experimental validation in high glucose-treated macrophages and human DFU tissues confirmed their reduced expression at both transcriptional and protein levels, particularly noting marked loss of EEF1A1 in epidermal layers and infiltrating CD68+ macrophages. Direct measurement of lysine lactylation (Kla) confirmed increased global lactylation under diabetic conditions. Conclusion: This study identifies CHD4, EEF1A1, and EEF1G as key lactylation-related genes involved in DFU progression, with significant classificational potential and close links to immune microenvironment dysregulation. These findings highlight lactylation as a promising regulatory mechanism in diabetic wound pathology and support further development of lactylation-targeted biomarkers and therapeutic strategies for DFU management, and require external validation and functional mechanistic studies.