{"database":"iProX","file_versions":[],"scores":null,"additional":{"omics_type":["Proteomics"],"submitter":["Min Hu"],"species":["Mus Musculus"],"full_dataset_link":["http://www.iprox.org/page/project.html?id=IPX0013771000"],"submitter_email":["humin@jlu.edu.cn"],"submitter_affiliation":["Hospital of Stomatology, Jilin University"],"sample_protocol":[""],"repository":["iProX"],"data_protocol":[""],"pubmed_abstract":["Hyperlipidemic periodontitis (HPD) represents a prevalent comorbidity linking systemic metabolic dysregulation with local inflammation, yet the microbial mechanisms driving this gut-oral crosstalk remain elusive. Here, the comorbid state of HPD is linked to hyperlipidemia-associated gut microbiota changes, which are prominently accompanied by the depletion of Odoribacter splanchnicus in both patients and mice. Fecal microbiota transplantation demonstrates that this gut dysbiosis exacerbates periodontal destruction when local inflammation is present. Mechanistically, intragastric administration of live O. splanchnicus ameliorates HPD by remodeling the gut ecosystem and upregulating the metabolite β-guanidinopropionic acid (β-GPA). Notably, direct supplementation with β-GPA reproduces these protective effects. Furthermore, β-GPA is proposed as a systemic effector linking the gut and periodontal tissues, where its protective effect is associated with the suppression of the pro-inflammatory Toll-like receptor 4 (TLR4) signaling cascade. These findings highlight a link involving O. splanchnicus, β-GPA, and the modulation of TLR4 signaling, offering a potential microbiome-based therapeutic strategy for managing complex metabolic-inflammatory comorbidities."],"pubmed_title":["Gut commensal Odoribacter splanchnicus attenuates hyperlipidemic periodontitis via gut-oral metabolic transmission of β-GPA."],"pubmed_authors":["Xu Jing J, Han Ziyi Z, Xue Qing Q, Wang Haoran H, Li Yutong Y, Song Jiyu J, Li Lanzhou L, Hu Min M, Wang Di D"],"additional_accession":[]},"is_claimable":false,"name":"Proteomic analysis of periodontal tissue reveals β-guanidinopropionic acid (β-GPA) mediated inhibition of the TLR4 pathway in a mouse model of hyperlipidemic periodontitis.","description":"This project aims to elucidate the molecular mechanisms by which the gut microbial metabolite β-guanidinopropionic acid (β-GPA) alleviates hyperlipidemic periodontitis (HPD). We performed Tandem Mass Tag (TMT) based quantitative proteomic analysis on periodontal tissues from HPD model mice versus those treated with β-GPA. The goal was to identify key differentially expressed proteins and uncover the protective signaling pathways modulated by β-GPA, ultimately identifying the TLR4-MyD88 axis as a primary therapeutic target.","dates":{"publication":"Mon Oct 13 00:00:00 GMT+01:00 2025"},"accession":"PXD069376","cross_references":{"TAXONOMY":["10090"],"pubmed":["42277050"]}}