1Department of Medical and Surgical Sciences, Fondazione Policlinico Universitario Agostino Gemelli IRCCS, Rome, Italy
2Department of Translational Medicine and Surgery, Università Cattolica del Sacro Cuore, Università Cattolica del Sacro Cuore, Rome, Italy
3Department of Medical and Surgical Sciences, UOC CEMAD Centro Malattie dell'Apparato Digerente, Medicina Interna e Gastroenterologia, Fondazione Policlinico Universitario Agostino Gemelli IRCCS, Rome, Italy
4Department of Internal Medicine I, Gastroenterology, Hepatology, Endocrinology & Metabolism, Medical University of Innsbruck, Innsbruck, Austria
Atherosclerosis reflects a chronic inflammatory process of arteries. The origin of chronic vascular inflammation has been associated over a long time primarily with lipid disorders, but evidence from the past years has suggested that lipid-independent pathways are also involved. Recent research has demonstrated that the gastrointestinal microbiota has an impact on the development of atherosclerosis. Many clinical studies have revealed that there exist altered gut microbiota and increased intestinal abundance of bacteria from the oral cavity in atherosclerosis-related disorders such as cardiovascular disease or stroke, while several studies have demonstrated insights into underlying mechanisms. Various microbial-derived metabolites, such as the pathogen-associated molecular pattern endotoxin, trimethylamine N-oxide or imidazole propionate, contribute to atherosclerosis, while other bacterial metabolites, such as some tryptophan derivatives, might be protective. Furthermore, gut microbiota and lipid pathways are highly interactive, and the gut microbiota affects lipid absorption and storage, and the gut microbiota also contributes to vascular ageing. Interference with the gut microbiota by prebiotics, probiotics and antibiotics has demonstrated beneficial effects on atherosclerosis mainly in preclinical models. Overall, the gut microbiota has appeared as an important rheostat for vascular inflammation in atherosclerosis, which is controlled by host-microbe interactions that may be therapeutically exploited in the future.
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Contributors WF, GI and HT wrote the initial draft of the manuscript. All authors (WF, TEA, GC, AG, GI, HT) revised and edited the manuscript for intellectual content and approved the final manuscript.
Funding GI was supported by the Ricerca Finalizzata Giovani Ricercatori 2018 (project GR-2018-12365734) and by the PNRR 2023 (project PNRR-POC-2023-12377319) of the Italian Ministry of Health, by the Next Gen Clinician Scientist 2024 of the AIRC (project 30203), by the Fondo Italiano per la Scienza of the Italian Ministry of Research (project FIS00001711). GI was supported by the Ricerca Finalizzata Giovani Ricercatori 2018 (project GR-2018-12365734) and by the PNRR 2023 (project PNRR-POC-2023-12377319) of the Italian Ministry of Health, by the Next Gen Clinician Scientist 2024 of the AIRC (project 30203), by the Fondo Italiano per la Scienza of the Italian Ministry of Research (project FIS00001711).
Competing interests None declared. HT is an associate editor of the journal.
Provenance and peer review Commissioned; internally peer reviewed.
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