Intestinal Microbiota Metabolism and Atherosclerosis

Liu, Tian-xing; Niu, Haitao; Zhang, Shuyang

doi:10.4103/0366-6999.167362

Cited by 39 publications

(27 citation statements)

References 57 publications

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“…The same finding was reported for M. luminyensis [129]. In fact, M. luminyensis was shown to be able to degrade trimethylamine (TMA), a compound associated with metabolic disorders such as trimethylaminuria [130], as well as reducing trimethylamine-N-oxide (TMAO) plasma levels, preventing the development of cardiovascular and chronic kidney diseases [131,132]. Thus, a potential use of M. luminyensis as an archaeal probiotic, or "archaebiotic", was proposed to promote a positive effect of archaea on human health [133].…”

Section: Human Archaeomesupporting

confidence: 71%

Gut Microbiota beyond Bacteria—Mycobiome, Virome, Archaeome, and Eukaryotic Parasites in IBD

Matijašić

Meštrović

Paljetak

et al. 2020

IJMS

189

110

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The human microbiota is a diverse microbial ecosystem associated with many beneficial physiological functions as well as numerous disease etiologies. Dominated by bacteria, the microbiota also includes commensal populations of fungi, viruses, archaea, and protists. Unlike bacterial microbiota, which was extensively studied in the past two decades, these non-bacterial microorganisms, their functional roles, and their interaction with one another or with host immune system have not been as widely explored. This review covers the recent findings on the non-bacterial communities of the human gastrointestinal microbiota and their involvement in health and disease, with particular focus on the pathophysiology of inflammatory bowel disease.

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Section: Human Archaeomesupporting

confidence: 71%

Gut Microbiota beyond Bacteria—Mycobiome, Virome, Archaeome, and Eukaryotic Parasites in IBD

Matijašić

Meštrović

Paljetak

et al. 2020

IJMS

189

110

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“…The associations of TMAO and the risk of CVDs have been reviewed previously; however, these studies did not aim to perform a meta‐analysis to quantify the risks of TMAO and its precursors for MACE. We observed the highly consistent positive associations between TMAO levels and the outcomes across studies, even among studies with low (<5.0 μmol/L) concentrations of TMAO at baseline, particularly after excluding the data among blacks.…”

Section: Discussionmentioning

confidence: 99%

Gut Microbiota Metabolites and Risk of Major Adverse Cardiovascular Disease Events and Death: A Systematic Review and Meta‐Analysis of Prospective Studies

Heianza

Manson

et al. 2017

JAHA

422

300

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BackgroundGut microbial metabolites have been implicated as novel risk factors for cardiovascular events and premature death. The strength and consistency of associations between blood concentrations of the gut microbial metabolites, trimethylamine‐N‐oxide (TMAO) and its precursors, with major adverse cardiovascular events (MACE) or death have not been comprehensively assessed. We quantified associations of blood concentrations of TMAO and its precursors with risks of MACE and mortality.Methods and ResultsPubMed and Embase databases were searched up, and a total of 19 prospective studies from 16 publications (n=19 256, including 3315 incident cases) with quantitative estimates of the associations of TMAO with the development of MACE or death were included in our main analysis. Multivariate‐adjusted relative risks (RRs) were used when these were available. Elevated concentrations of TMAO were associated with a pooled RR of 1.62 (95% CI, 1.45, 1.80; P heterogeneity=0.2; I2=23.5%) for MACE compared with low TMAO levels, and 1 study of black participants influenced the heterogeneity of the association. After excluding the data of blacks, the RRs were not different according to body mass index, prevalence of diabetes mellitus, history of cardiovascular diseases, and kidney dysfunction. Furthermore, elevated TMAO concentrations were associated with a pooled RR of 1.63 (1.36, 1.95) for all‐cause mortality. Individuals with elevated concentrations of TMAO precursors (l‐carnitine, choline, or betaine) had an approximately 1.3 to 1.4 times higher risk for MACE compared to those with low concentrations.ConclusionsElevated concentrations of TMAO and its precursors were associated with increased risks of MACE and all‐cause mortality independently of traditional risk factors.

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“…Firmicutes including Anaerococcus, Clostridium, Desulfitobacterium, Enterococcus, Streptococcus, and Proteobacteria including Dseulfovibrio, Enterobacter, Escherichia, Klebsiella, Proteus, Pseudomonas, Actinobacter, and Citrobacter have been associated with TMA production [100]. One study found that 8 species from Firmicutes and Proteobacteria consumed > 60% of choline for TMA production: Anaerococcus hydrogenalis, Clostridium asparagiforme, C. hathawayi, C. sporogenes, Escherichia fergusonii, Proteus penneri, Providencia rettgeri, and Edwardsiella tarda [103]. Other gut microbiota associated with higher TMAO production include Akkermansia, Sporobacter, Prevotella [95], and Ruminococcus gnavus [104], which are associated with atherosclerotic CAD.…”

Section: Trimethylamine-n-oxide Productionmentioning

confidence: 99%

Gut microbiota and cardiovascular disease: opportunities and challenges

et al. 2020

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Coronary artery disease (CAD) is the most common health problem worldwide and remains the leading cause of morbidity and mortality. Over the past decade, it has become clear that the inhabitants of our gut, the gut microbiota, play a vital role in human metabolism, immunity, and reactions to diseases, including CAD. Although correlations have been shown between CAD and the gut microbiota, demonstration of potential causal relationships is much more complex and challenging. In this review, we will discuss the potential direct and indirect causal roots between gut microbiota and CAD development via microbial metabolites and interaction with the immune system. Uncovering the causal relationship of gut microbiota and CAD development can lead to novel microbiome-based preventative and therapeutic interventions. However, an interdisciplinary approach is required to shed light on gut bacterial-mediated mechanisms (e.g., using advanced nanomedicine technologies and incorporation of demographic factors such as age, sex, and ethnicity) to enable efficacious and high-precision preventative and therapeutic strategies for CAD. Key points The causal relationship between gut microbiota and CAD development has yet to be confirmed. It is imperative to understand the potential direct and indirect causal roots between gut microbiota and CAD development via microbial metabolites and interaction with the immune system. Dynamic elements including our diet and demographic factors such as age, sex, and ethnicity can also affect our gut microbiota and CAD development and complicate this matter. Interdisciplinary approaches are required to shed light on the factors involved in the modulation of gut microbiota and its association with CAD development. Elucidating the system-level multifaceted web of factors involved in microbiome-mediated mechanisms and human health and disease can guide novel preventative and therapeutic interventions for CAD.

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Intestinal Microbiota Metabolism and Atherosclerosis

Cited by 39 publications

References 57 publications

Gut Microbiota beyond Bacteria—Mycobiome, Virome, Archaeome, and Eukaryotic Parasites in IBD

Gut Microbiota beyond Bacteria—Mycobiome, Virome, Archaeome, and Eukaryotic Parasites in IBD

Gut Microbiota Metabolites and Risk of Major Adverse Cardiovascular Disease Events and Death: A Systematic Review and Meta‐Analysis of Prospective Studies

Gut microbiota and cardiovascular disease: opportunities and challenges

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