ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025
The Type III Secretion System (T3SS) of Escherichia Coli Promotes Atherosclerosis in Type 2 Diabetes Mellitus.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Identification of Pinostilbene as a natural STING agonist that triggers FTH1 degradation via K48-ubiquitination to induce ferroptosis in non-small cell lung cancer.Redox biology · 2026Article
- Article
- Leonurine ameliorates experimental type 2 diabetes through gut microbiota remodeling, enhanced butyrate production, and MPC2 activation to restore GLP-1 secretion.Frontiers in pharmacology · 2026Article
- The Type III Secretion System (T3SS) of Escherichia Coli Promotes Atherosclerosis in Type 2 Diabetes Mellitus.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
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16 authors.
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Abstract
Large-scale studies indicate a strong relationship between the gut microbiome, type 2 diabetes mellitus (T2DM), and atherosclerotic cardiovascular disease (ASCVD). Here, a higher abundance of the type III secretion system (T3SS) virulence factors of Enterobacteriaceae/Escherichia-Shigella in patients with T2DM-related-ASCVD, which correlates with their atherosclerotic stenosis is reported. Overexpression of T3SS via Citrobacter rodentium (CR) infection in Apoe-/- T2DM mice exacerbated atherosclerotic lesion formation and increased gut permeability. Non-targeted metabolomic and proteomic analysis of mouse serum showed that T3SS caused abnormal glycerophospholipid metabolism in mice. Proteomics, RNA sequencing, and functional analyses showed that T3SS induced ferroptosis in intestinal epithelial cells, partly due to increased expression of ferritin heavy chains (FTH1). This findings first demonstrated that T3SS increases ferroptosis in intestinal epithelial cells, via disrupting the intestinal barrier and upregulation of phosphatidylcholine, thereby exacerbating T2DM-related ASCVD.
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