Burns最新文献

Background: Keloids are benign fibrous lesions characterized by tumor-like behavior, including continuous expansion beyond the original wound boundaries, absence of natural regression, and a strong tendency to recur after treatment. While cellular heterogeneity and intercellular signaling are recognized contributors to keloid progression, the specific phenotypic transitions and regulatory interactions among involved cell types remain poorly defined.

Methods: We analyzed transcriptomic profiles from six samples in the GSE163973 dataset, including three keloid and three normal scar tissues. Single-cell RNA sequencing datasets were analyzed to classify cellular populations and to investigate gene expression patterns and ligand-receptor interactions within distinct subgroups.

Results: Nine primary cell types were identified: endothelial cells, fibroblasts, smooth muscle cells/pericytes, keratinocytes, macrophage/dendritic cells, lymphatic endothelial cells, T cells, Schwann cells, and melanocytes. Among these, endothelial cells and Schwann cells showed the greatest transcriptional variability. Subcluster analysis and ligand-receptor mapping revealed pronounced heterogeneity and complex intercellular communication within keloid tissues. Notably, one subcluster of keloid endothelial cells shared transcriptional features with endothelial cells in cutaneous malignant tumors and demonstrated strong migratory potential. PLPP3 was identified as a key regulator of endothelial tubulogenesis within this subpopulation.

Conclusion: This study highlights the distinct heterogeneity and dynamic intercellular interaction between endothelial cells (ECs) and Schwann cells (SCs) in the pathogenesis of keloids. The identification of tumor-like endothelial subclusters and their regulatory networks provides novel insights into keloid biology and suggests PLPP3 as a potential target for therapeutic intervention.

Diabetic wounds (DWs) are characterized by impaired angiogenesis, which is a key factor contributing to delayed wound healing. However, the specific regulators of angiogenic dysfunction in DWs remain poorly understood. In this study, we identified the abnormal downregulation of tissue inhibitor of metalloproteinases 2 (TIMP2) in skin wounds of diabetic patients through RNA sequencing and histopathological techniques. By upregulating TIMP2 expression via adeno-associated virus (AAV) transfection in vitro and in vivo, we demonstrated that TIMP2 overexpression enhanced vascular endothelial cell proliferation through activation of the PI3K-AKT signaling pathway and promoted wound healing in diabetic mice. Furthermore, using multiple online functional prediction databases and dual luciferase reporter assays, we investigated miR-106a-5p as an upstream regulator of TIMP2, which was upregulated in the wounds of diabetic mice. Inhibition of miR-106a-5p can upregulate TIMP2 mRNA expression in vascular endothelial cells, leading to increased cell proliferation and decreased apoptosis, thereby accelerating wound healing in diabetic mice. Our findings underscore the critical role of the TIMP2 and its upstream regulator miR-106a-5p in angiogenesis during wound healing, providing a promising avenue for diabetic wound repair.

Background: Burn injuries place a high burden on low- and middle-income countries (LMICs), accounting for over 90% of global fire-related deaths. As survival improves, the metric for successful care has shifted to health-related quality of life (HRQoL). Recovery in LMICs is compounded by limited rehabilitation access, poverty, and social stigma. This systematic review synthesizes evidence on HRQoL outcomes and their predictors among burn survivors in LMICs.

Methods: Following PRISMA 2020 guidelines, we systematically searched PubMed/MEDLINE, Cochrane, and regional databases (2013-2025) across Asian, African, and Middle Eastern LMICs. We included quantitative studies (cross-sectional, cohorts, randomized controlled trials [RCTs]) using validated HRQoL instruments. Studies were limited to 15 days to 3 months post-injury/discharge. Due to measurement heterogeneity, a full meta-analysis was precluded, but a targeted comparative analysis using standardized mean differences was performed on four intervention comparisons.

Results: The search yielded 721 records, with 10 studies included from South Asia, Africa, and the Middle East. The review identified consistently markedly impaired HRQoL, with the most compromised domains being physical functioning and psychological well-being. Key predictors of poor HRQoL included greater burn severity (e.g., ≥20% TBSA, third-degree burns) and crucial socioeconomic factors. Limited interventional data demonstrated that targeted physical rehabilitation, self-care education, and low-cost, remote delivery models significantly improved short-term scores. The targeted comparative analysis revealed a moderate-to-large standardized effect on HRQoL scores (Cohen's d ranging from 1.51 to 3.81) favoring rehabilitation interventions.

Conclusion: HRQoL is severely compromised among burn survivors in LMICs, driven by clinical severity and exacerbated by socioeconomic barriers. Promising, scalable, low-cost rehabilitation programs can meaningfully improve short-term outcomes. Future research must prioritize standardized core outcome sets and policies should focus on integrating essential mental health and social support into long-term care frameworks.