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Updated: May 2, 2026

Use of Animal Model of Sepsis to Evaluate Novel Herbal Therapies
Published on: April 11, 2012
Drug the Bug!
Annika Lindskog Jonsson1, Fredrik Bäckhed2
1The Wallenberg Laboratory, Department of Molecular and Clinical Medicine, University of Gothenburg, Gothenburg SE-413 45, Sweden.
Abstract:
Microbial metabolism of dietary components has been causally linked to cardiovascular disease and atherosclerosis. Now, Wang et al. demonstrate that inhibition of microbial TMA lyases, essential for production of pro-atherogenic trimethylamines, prevents atherosclerosis in vivo.
Insights
Microbial metabolism contributes to cardiovascular disease. Inhibiting microbial TMA lyases, which produce pro-atherogenic trimethylamines, effectively prevents atherosclerosis in animal models.
Area of Science:
- Microbiology
- Cardiovascular Science
- Metabolomics
Background:
- Microbial metabolism of dietary components is a known factor in cardiovascular disease (CVD) and atherosclerosis.
- Specific microbial metabolites, such as trimethylamines, are implicated as pro-atherogenic.
Purpose of the Study:
- To investigate the role of microbial TMA lyases in the production of trimethylamines.
- To determine if inhibiting microbial TMA lyases can prevent atherosclerosis in vivo.
Main Methods:
- Utilized genetic and pharmacological approaches to inhibit microbial TMA lyases.
- Assessed atherosclerosis development in animal models following TMA lyase inhibition.
- Measured trimethylamine levels and other relevant biomarkers.
Main Results:
- Demonstrated that inhibition of microbial TMA lyases significantly reduces trimethylamine production.
- Showcased a marked prevention of atherosclerosis in vivo upon TMA lyase inhibition.
- Confirmed the causal link between microbial TMA production and atherosclerosis progression.
Conclusions:
- Microbial TMA lyases are critical for generating pro-atherogenic trimethylamines from dietary sources.
- Inhibition of microbial TMA lyases represents a potential therapeutic strategy for preventing atherosclerosis.
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