Qin Qi, Haba Daijiro, Takizawa Chihiro, Tomida Sanai, Horinouchi Ai, Katagiri Mikako, Nomura Seitaro, Nakagami Gojiro
Department of Gerontological Nursing/Wound Care Management, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Global Nursing Research Center, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Wound Repair Regen. 2025 May-Jun;33(3):e70038. doi: 10.1111/wrr.70038.
Wound healing is often hindered by hyperglycemia, chronic inflammation and ageing. Despite extensive research on the pathophysiology of hard-to-heal wounds, wound healing remains complex and poses challenges in treatment and management. Current wound treatments and care mostly target a single pathology, such as infection, while most hard-to-heal wounds are multifactorial. Therefore, exploring the factors that do not rely on a single pathology is crucial to fill the gap in current wound management. Despite containing more comprehensive information than commonly used wound tissue samples, cells in the wound fluid have not drawn much attention because of collection difficulties. This study aimed to use single-cell RNA sequencing (scRNA-seq) of cells from wound fluid to identify specific biomarkers for hard-to-heal wounds, with the hypothesis that common biomarkers among various wound models can be potentially applied to complex hard-to-heal wounds in clinical settings. Three representative delayed wound models, aged, diabetic and lipopolysaccharide-induced inflammatory wound models, were compared with normal young mice to explore commonly shared genes that exist in different pathological delayed wound healing models. The shared upregulation of cell cycle and cellular senescence-related genes such as Rpl11, Rpl26, Rps3, Rps15, Rps 20, Rps26, Ccl2, Cdk2ap2 and Ccnd3 and the downregulation of immune response regulation genes such as Tnfaip3, Junb, Il1r2, Plaur, Il1rn, Il1a, Cxcl2, Cd14, S100a8 and S100a9 in all delayed healing wound models were found in most immune cell subgroups, especially the macrophage subgroup. The results of this study suggested cellular senescence of cells in wound fluid could be related to hard-to-heal wounds.
伤口愈合常常受到高血糖、慢性炎症和衰老的阻碍。尽管对难愈合伤口的病理生理学进行了广泛研究,但伤口愈合仍然很复杂,在治疗和管理方面面临挑战。目前的伤口治疗和护理大多针对单一病理状况,如感染,而大多数难愈合伤口是多因素的。因此,探索不依赖单一病理状况的因素对于填补当前伤口管理的空白至关重要。尽管伤口液中的细胞比常用的伤口组织样本包含更全面的信息,但由于采集困难,尚未引起太多关注。本研究旨在对伤口液中的细胞进行单细胞RNA测序(scRNA-seq),以识别难愈合伤口的特定生物标志物,假设各种伤口模型中的共同生物标志物可能适用于临床环境中的复杂难愈合伤口。将三种代表性的延迟伤口模型,即老年、糖尿病和脂多糖诱导的炎症伤口模型,与正常年轻小鼠进行比较,以探索在不同病理延迟伤口愈合模型中存在的共同基因。在大多数免疫细胞亚群中,尤其是巨噬细胞亚群中,发现所有延迟愈合伤口模型中细胞周期和细胞衰老相关基因如Rpl11、Rpl26、Rps3、Rps15、Rps20、Rps26、Ccl2、Cdk2ap2和Ccnd3的共同上调,以及免疫反应调节基因如Tnfaip3、Junb、Il1r2、Plaur、Il1rn、IlIa、Cxcl2、Cd14、S100a8和S100a9的下调。本研究结果表明,伤口液中细胞的衰老可能与难愈合伤口有关。