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Table_2_Dysbiosis of Gut Microbiota and Metabolite Phenylacetylglutamine in Coronary Artery Disease Patients With Stent Stenosis.pdf

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NIAID Data Ecosystem2026-03-13 收录
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https://figshare.com/articles/dataset/Table_2_Dysbiosis_of_Gut_Microbiota_and_Metabolite_Phenylacetylglutamine_in_Coronary_Artery_Disease_Patients_With_Stent_Stenosis_pdf/19417403
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IntroductionDysbiotic gut microbiota (GM) plays a regulatory role during the pathogenesis of several cardiovascular diseases, including atherosclerosis. GM-derived metabolite phenylacetylglutamine (PAGln) enhances platelet responsiveness and thrombosis potential, thereby inducing major adverse cardiovascular events. However, the role of GM and microbial metabolite PAGln in the pathogenesis of in-stent stenosis remains unknown. Methods16S rRNA sequencing was performed on fecal samples in 103 coronary artery disease (CAD) patients, including 35 individuals with in-stent patency (control), 32 individuals with in-stent hyperplasia (ISH), and 36 subjects with in-stent stenosis (ISS), and the levels of plasma PAGln were evaluated by enzyme-linked immunosorbent assay. ResultsThe results revealed significantly enhanced microbial diversity and disrupted composition, such as enrichment of Roseburia, Blautia, and Ruminococcus, were observed in CAD patients with in-stent stenosis. The imbalance of microbial function related to PAGln synthesis and elevated plasma GM-derived metabolite PAGln levels was detected in CAD patients with in-stent stenosis. The GM-dependent diagnostic model could identify CAD patients with in-stent stenosis. ConclusionThe current study revealed the disordered signature, altered functions, and potential diagnostic ability of GM in CAD patients with in-stent hyperplasia and stenosis. Enhanced microbiota-derived PAGln synthesis-related functions and elevated plasma PAGln levels were associated with in-stent stenosis and hyperplasia in CAD patients. Thus, an intervention targeting gut microbes may be a promising strategy to prevent stent stenosis in patients with CAD.
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2022-03-25
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