Wu Zimei, Hou Qiaodan, Chi Heng, Liu Jihong, Mei Yixin, Chen Tingting, Yang Kunkun, Zheng Jingna, Xu Jing, Wei Fuxin, Wang Lin
School of Medicine, Southern University of Science and Technology, Shenzhen, Guangdong 518055, China.
Department of Orthopedic Surgery, The Seventh Affiliated Hospital of Sun Yat-sen University, Shenzhen, Guangdong 518107, China.
Genes Dis. 2023 Oct 17;11(6):101145. doi: 10.1016/j.gendis.2023.101145. eCollection 2024 Nov.
The pathogenic effects of type 2 diabetes on bone tissue are gaining attention, but the cellular and molecular mechanisms underlying osteoimmunology are still unclear in diabetes-related bone diseases. We delineated the single-cell transcriptome of bone marrow cells from both wide type and type 2 diabetes mice, which provided the first detailed global profile of bone marrow cells and revealed a distinct bone immune microenvironment at the genetic level under type 2 diabetic condition. It was observed that osteoclast activity was inhibited due to a dysregulated cytokine network, which ultimately led to decreased osteoclast formation and differentiation. In type 2 diabetes mice, a specific cluster (cluster 18, monocytes/macrophages 2) was identified as the precursor of osteoclasts with diminished differentiation potential. was demonstrated to be the key transcription factor in the underlying mechanism.
2型糖尿病对骨组织的致病作用正日益受到关注，但在糖尿病相关骨疾病中，骨免疫学的细胞和分子机制仍不清楚。我们描绘了野生型和2型糖尿病小鼠骨髓细胞的单细胞转录组，这提供了骨髓细胞的首个详细整体概况，并在基因水平上揭示了2型糖尿病条件下独特的骨免疫微环境。据观察，由于细胞因子网络失调，破骨细胞活性受到抑制，最终导致破骨细胞形成和分化减少。在2型糖尿病小鼠中，一个特定的细胞簇（细胞簇18，单核细胞/巨噬细胞2）被确定为分化潜能降低的破骨细胞前体。被证明是潜在机制中的关键转录因子。
