Scar tissue is the inevitable result of repairing human skin after it has been subjected to external destructive stimuli. It leads to localized damage to the appearance of the skin, accompanied by symptoms such as itching and pain, which reduces the quality of life of the patient and causes serious medical burdens. With the continuous development of economy and society, there is an increasing demand for beauty. People are looking forward to a safer and more effective method to eliminate pathological scarring. In recent years, adipose-derived stem cells (ADSCs) have received increasing attention from researchers. It can effectively improve pathological scarring by mediating inflammation, regulating fibroblast proliferation and activation, and vascular reconstruction. This review focuses on the pathophysiological mechanisms of hypertrophic scarring, summarizing the therapeutic effects of in vitro, in vivo, and clinical studies on the therapeutic effects of ADSCs in the field of hypertrophic scarring prevention and treatment, the latest application techniques, such as cell-free therapies utilizing ADSCs, and discussing the advantages and limitations of ADSCs. Through this review, we hope to further understand the characterization of ADSC and clarify the effectiveness of its application in hypertrophic scarring treatment, so as to provide clinical guidance.

Increasing evidence suggests a potential causal association between lipid levels and facial aging. The aim of this study was to investigate the relationship between levels of specific lipids and facial aging via Mendelian randomization methods. Additionally, this study aimed to identify mediators and explore relevant genes and drug targets. In this study, genome-wide association data on plasma lipids from 7,174 Finnish individuals in the UK Biobank were used. Two-sample Mendelian randomization was applied to assess the causal effects of specific lipids on facial aging. Sensitivity and pleiotropy analyses were conducted to ensure the robustness and reliability of the results. Multivariate Mendelian randomization was conducted to account for the potential impact of confounding factors. Furthermore, summary-data-based Mendelian randomization was used to identify relevant genes, which were validated through multiomics data. Finally, drug‒gene interactions were explored via molecular docking techniques. Two-sample Mendelian randomization analysis revealed a causal relationship between lipid levels and facial aging. According to the multivariate Mendelian randomization results, smoking was found to mediate this association, and these lipids remained significantly associated with facial aging, even after accounting for environmental confounders. Using summary-data-based Mendelian randomization, CYP21A2, CCND1, PSMA4, and MED1 were identified as potential gene targets, with MED1 further validated through pQTL and mQTL data. Additionally, the MED1 protein was found to bind spontaneously with astragalin, fenofibrate, and ginsenoside. The results revealed a causal relationship between lipid levels and facial aging, revealing key gene targets that were still significantly associated with facial aging after controlling for environmental confounders. Additionally, the interactions between MED1 and certain drugs may indicate potential pathways for therapeutic interventions related to facial aging.

Background: Non-syndromic cleft lip with or without cleft palate (NSCL/P) accounts for 70% of orofacial cleft cases worldwide and causes physical dysfunction and psychological burden. Prior bibliometric studies have outlined the general NSCL/P research landscape; however, a systematic overview targeting the genetic dimension, evolutionary trends since the Human Genome Project, and dual-database cross-validation remains limited. This study mapped the global bibliometric landscape of NSCL/P genetics, identified shifting research paradigms, and functionally validated candidate genes through bioinformatic analyses of environmental risk factors. Methods: Publications from January 1990 to 31 January 2026, were retrieved from the Web of Science Core Collection and analyzed using bibliometric tools, including R-Bibliometrix, VOSviewer, and CiteSpace. Subsequently, Scopus publications were searched using the same search strategy for cross-validation. Finally, toxicant-induced and NSCL/P-related genes were screened from the GeneCards database to identify overlapping targets, followed by construction of a protein–protein interaction network and Kyoto Encyclopedia of Genes and Genomes enrichment analysis to characterize potential functional pathways. Results: A total of 1,511 eligible publications were analyzed, covering 86 countries and regions, 1,766 institutions, 6,061 authors, and 383 journals, with rapid publication growth observed between 2018 and 2021. The United States led in output and citations alongside the University of Iowa and Murray, Jeffrey C., as key contributors. Keyword clustering categorized the current studies into four major categories: genetic analysis methodologies, developmental biology and phenotypes, epidemiology and environmental factors, and molecular regulatory mechanisms. Alcohol- and nicotine-induced overlapping pathogenic genes were identified with enriched pathways involved in the regulation of embryonic craniofacial development, cell proliferation, and apoptosis. Conclusion: This study clarified the publication trends, key research forces, disciplinary distributions, and hotspots in NSCL/P genetics, revealing an ongoing shift in research focus. In silico network analyses of public databases identified distinct molecular pathways mediating alcohol- and nicotine-induced developmental disorders. These findings provide reliable evidence for future mechanistic exploration of NSCL/P pathogenesis.