Document Type : Review Article
Authors
1
Department of Nuclear Medicine, School of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran
2
Ionizing and Non-Ionizing Radiation Protection Research Center (INIRPRC), School of Paramedical Sciences, Shiraz University of Medical Sciences, Shiraz, Iran
3
Molecular Dermatology Research Center, Shiraz University of Medical Sciences, Shiraz, Iran
4
Research Center for Traditional Medicine and History of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran
5
Department of Medical Journalism, School of Paramedical Sciences, Shiraz University of Medical Sciences, Shiraz, Iran
6
School of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran
7
Department of Prosthodontics, School of Dentistry, Tehran University of Medical Sciences, Tehran, Iran
Abstract
Atherosclerosis, a chronic inflammatory disease affecting large arteries, is the most prevalent cause of cardiovascular events. Dysbiosis refers to an imbalance in gut microbiota composition. This narrative review was compiled by searching the PubMed, Scopus, Google Scholar, and Embase databases, utilizing scientific articles published between 2000 and 2025. Studies indicated that gut microbiota dysbiosis contributes to atherosclerosis through the regulation of metabolic, immune, and inflammatory pathways. Dysbiosis promotes low-grade systemic inflammation by increasing intestinal permeability and the translocation of lipopolysaccharides into the circulation. Additionally, it reduces the production of short-chain fatty acids, impairing endothelial function and mucosal barrier integrity. Meanwhile, trimethylamine-N-oxide (TMAO) produced by these bacteria exacerbates atherosclerosis through activation of nuclear factor kappa B (NF-κB) and the Nlrp3 inflammasome, inhibition of reverse cholesterol transport and bile acid synthesis, induction of endoplasmic reticulum stress, foam cell formation, and increased platelet reactivity. Altered bile acid signaling due to dysbiosis amplifies vascular inflammation. Following dysbiosis, bile acid signaling is altered via the farnesoid X receptor (FXR) and TGR5, leading to intensified vascular inflammation. Clinical data revealed distinct microbial patterns in patients with coronary atherosclerosis, as well as an association between TMAO levels and adverse cardiovascular outcomes. Nutritional interventions, probiotics, fecal microbiota transplantation, and exercise hold promise as novel preventive and therapeutic strategies.
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