牙周炎
转录组
生物
免疫系统
计算生物学
串扰
基因
牙龈卟啉单胞菌
转录因子
疾病
免疫学
遗传学
生物信息学
牙病
基因调控网络
信号转导
基因表达调控
基因表达
抄写(语言学)
牙周病原体
转录调控
RNA序列
炎症
基因表达谱
候选基因
狼疮性肾炎
核糖核酸
细胞生物学
先天免疫系统
多发性硬化
作者
Zhongxuan Zhang,Zihan Ma,Ruidong Zhang,Min Ye,Zhongyu Shi,Miao Yu,Lingling Ou
标识
DOI:10.1038/s41540-026-00690-7
摘要
Periodontitis (PD) and metabolic dysfunction-associated steatotic liver disease (MASLD) were highly prevalent inflammatory disorders that frequently coexisted, yet the molecular basis of their comorbidity remained poorly defined. Here, we applied an integrative multi-omics strategy that combined bulk RNA sequencing, weighted gene co-expression network analysis, spatial transcriptomics, single-cell profiling, and machine learning. This approach identified 11 hub genes bridging immune activation and metabolic remodeling, among which Annexin A6 (ANXA6) emerged as a key cross-disease candidate. Spatial transcriptomics supported tissue-specific localization of the hub-gene signature, while single-cell analysis revealed selective enrichment of ANXA6 expression in γδ T cells. Notably, ANXA6-high γδ T cells exhibited enhanced signaling interactions with endothelial cells, suggesting immune-vascular crosstalk in PD-MASLD comorbidity. Upstream regulatory analysis further highlighted transcription factors associated with ANXA6 expression, and Connectivity Map-based prediction suggested candidate compounds with the potential to reverse ANXA6-associated transcriptional programs. Collectively, these findings support the hypothesis that ANXA6-high γδ T cell-endothelial communication represents a shared immunological feature of PD-MASLD comorbidity, offering novel insights into common immune programs and potential therapeutic opportunities.
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