糖基化
节点2
炎症
生物
牙周炎
壁酰二肽
信号转导
愤怒(情绪)
受体
细胞生物学
糖基化终产物
NF-κB
炎症体
免疫学
癌症研究
内科学
医学
先天免疫系统
生物化学
神经科学
免疫系统
作者
Zhu-Ling Guo,Jie Zhou,Xue-Jing Lin,Qingxi Yuan,Yulei Dong,Qibing Liu,Tao Wang
标识
DOI:10.1016/j.yexcr.2024.113999
摘要
The heightened prevalence and accelerated progression of periodontitis in individuals with diabetes is primarily attributed to inflammatory responses in human periodontal ligament cells (HPDLCs). This study is aimed at delineating the regulatory mechanism of nucleotide-binding oligomerization domain-like receptors (NLRs) in mediating inflammation incited by muramyl dipeptide (MDP) in HPDLCs, under the influence of advanced glycation end products (AGEs), metabolic by-products associated with diabetes. We performed RNA-seq in HPDLCs induced by AGEs treatment and delineated activation markers for the receptor of AGEs (RAGE). It showed that advanced glycation end products modulate inflammatory responses in HPDLCs by activating NLRP1 and NLRP3 inflammasomes, which are further regulated through the NF-κB signaling pathway. Furthermore, AGEs synergize with NOD2, NLRP1, and NLRP3 inflammasomes to augment MDP-induced inflammation significantly.
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