ArticleNaunyn-Schmiedeberg's archives of pharmacology2026
Long-term artificial sweetener exposure increases the risk of atherosclerosis.
Article in Naunyn-Schmiedeberg's archives of pharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Authors and funding
7 authors.
Funding
Abstract
This study aimed to elucidate the potential molecular mechanisms by which artificial sweeteners contribute to the initiation and progression of atherosclerosis, with the goal of providing a theoretical basis for the safety evaluation of artificial sweeteners and the prevention and treatment of atherosclerosis. Targets associated with seven artificial sweeteners (aspartame, acesulfame, sucralose, NHDC, cyclamate, neotame, and saccharin) were retrieved from the CTD and ChEMBL databases. Additional target screening was performed using SwissTargetPrediction, SEA, TargetNet, and PharmMapper. Disease Ontology (DO) enrichment analysis was conducted to identify diseases potentially linked to artificial sweetener targets. Atherosclerosis-related targets were obtained from GeneCards, DisGeNET, and TTD databases, and their union was taken. Weighted gene coexpression network analysis (WGCNA) was applied to identify key modules associated with immune cell infiltration. Mendelian randomization (MR) was performed to identify core targets with potential causal effects. Single-sample GSEA and CellChat analyses were conducted for core targets. Finally, molecular docking and molecular dynamics simulations were used to evaluate the binding stability between core target proteins and artificial sweeteners. A total of 795 targets associated with the seven artificial sweeteners were identified. DO enrichment analysis revealed significant associations with atherosclerosis. Integration of targets from GeneCards, DisGeNET, and TTD yielded 2904 atherosclerosis-related targets. Intersection with 572 DEGs from GEO datasets identified 53 overlapping targets. Further intersection with WGCNA key module genes yielded 13 potential candidate targets. MR analysis indicated strong causal associations of SCARB1 and ST14 with atherosclerosis. Molecular docking and dynamics simulations confirmed stable binding between SCARB1/ST14 proteins and artificial sweeteners. Artificial sweeteners may promote the development and progression of atherosclerosis by modulating cholesterol metabolism via the SCARB1 target and influencing macrophage migration through the ST14 target.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.