Department of General Biology, Federal University of Viçosa, Viçosa 36570-900, Brazil.
Department of Structural Biology, Institute of Biomedical Sciences, Federal University of Alfenas, Alfenas 37130-001, Brazil.
Int J Mol Sci. 2024 Aug 19;25(16):8992. doi: 10.3390/ijms25168992.
Skin wounds, primarily in association with type I diabetes mellitus, are a public health problem generating significant health impacts. Therefore, identifying the main pathways/mechanisms involved in differentiating fibroblasts into myofibroblasts is fundamental to guide research into effective treatments. Adopting the PRISMA guidelines, this study aimed to verify the main pathways/mechanisms using diabetic murine models and analyze the advances and limitations of this area. The Medline (PubMed), Scopus, and Web of Science platforms were used for the search. The studies included were limited to those that used diabetic murine models with excisional wounds. Bias analysis and methodological quality assessments were undertaken using the SYRCLE bias risk tool. Eighteen studies were selected. The systematic review results confirm that diabetes impairs the transformation of fibroblasts into myofibroblasts by affecting the expression of several growth factors, most notably transforming growth factor beta (TGF-beta) and NLRP3. Diabetes also compromises pathways such as the SMAD, c-Jun N-terminal kinase, protein kinase C, and nuclear factor kappa beta activating caspase pathways, leading to cell death. Furthermore, diabetes renders the wound environment highly pro-oxidant and inflammatory, which is known as OxInflammation. As a consequence of this OxInflammation, delays in the collagenization process occur. The protocol details for this systematic review were registered with PROSPERO: CRD42021267776.
皮肤创伤,主要与 1 型糖尿病有关,是一个对公共健康造成重大影响的问题。因此,确定将成纤维细胞分化为肌成纤维细胞的主要途径/机制对于指导有效的治疗研究至关重要。本研究采用 PRISMA 指南,旨在通过糖尿病小鼠模型验证主要途径/机制,并分析该领域的进展和局限性。使用 Medline(PubMed)、Scopus 和 Web of Science 平台进行搜索。纳入的研究仅限于使用切创糖尿病小鼠模型的研究。使用 SYRCLE 偏倚风险工具进行偏倚分析和方法学质量评估。共选择了 18 项研究。系统评价结果证实,糖尿病通过影响几种生长因子(尤其是转化生长因子-β(TGF-β)和 NLRP3)的表达,损害成纤维细胞向肌成纤维细胞的转化。糖尿病还会损害 SMAD、c-Jun N-末端激酶、蛋白激酶 C 和核因子 κB 激活半胱氨酸蛋白酶途径等途径,导致细胞死亡。此外,糖尿病使创面环境高度氧化应激和炎症,这被称为 OxInflammation。由于这种 OxInflammation,胶原化过程会延迟。本系统评价的方案细节已在 PROSPERO 上注册:CRD42021267776。