Microbiome & Chronic Diseases

Evidence Based Medicine
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Disease ⇒ Atherosclerosis {40000106}

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Cardiovascular, Angiology, DietNutrition
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References Notes

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Shared Reference Notes

  • [1.8
    - Human blood platelets are a critical contributor to the hemostatic process and a crucial role in developing atherosclerosis and, finally, contribute to cardiac events. - Gut microbiota and their metabolites play an important role in systemic inflammation and modulate various CVD risk factors.
  • [1.9
    - Distinct members of the order Burkholderiales were present at high levels in all atherosclerotic plaques obtained from patients with atherosclerosis with the genus Curvibacter being predominant in all plaque samples. Moreover, unclassified Burkholderiales as well as members of the genera Propionibacterium and Ralstonia were typically the most significant taxa for all atherosclerotic plaques.
  • [1.10
    - Aortic atherosclerotic lesions were significantly reduced after F. nucleatum infection suggesting a potential protective function for this member of the oral microbiota.
  • [1.11
    -Clostridia (sensu stricto), bifidobacteria, and coriobacteria were significantly correlated with TMA production in the mixed fermentation system but did not produce notable quantities of TMA from TMAO in pure culture. - TMAO stimulated the growth of Enterobacteriaceae; these bacteria produced most TMA from TMAO. - Reduction of TMAO by the gut microbiota (predominantly Enterobacteriaceae) to TMA followed by host uptake of TMA into the bloodstream from the intestine and its conversion back to TMAO by host hepatic enzymes is an example of metabolic retroconversion. TMAO influences microbial metabolism depending on isolation source and taxon of gut bacterium.
  • [1.7
    - the abundance of #Roseburia intestinalis is negatively correlated with the size of atherosclerotic lesions in the mouse model of atherosclerosis. - when #Roseburia intestinalis was taken along with a high-fiber diet, aortic atherosclerotic plaques were reduced in size. This study suggests that the butyrate, a microbial metabolite, mediates these effects
  • [1.12] [#Coronary artery disease
    - #Bilophila, a genus of gut microbes, can metabolize #TMA, resulting in lower #TMAO,58 suggesting that differences in #TMA-metabolizing gut bacteria in individuals lead to different ultimate effects, and replacement of relevant bacteria may reduce the risk from #TMAO.
  • - #Butyrate has been shown to be a potential therapeutic strategy for atherosclerosis, specifically by its promoting cholesterol efflux through upregulation of ABCA1 expression in macrophages, thereby ameliorating atherosclerosis.
  • - #TMAO is the hepatic oxidation product of the microbial trimethylamine (#TMA). - dietary supplementation with #TMAO was shown to promote atherogenesis and development of atherosclerosis in mice. - #TMAO levels associate with an increased risk of adverse cardiovascular events. - Carotid atherosclerosis was demonstrated to be associated with gut microbial metabolites (especially #TMAO and #p-cresol sulfate) in >3,000 patients, which could serve as an independent predictor of the disease.
  • [1.13] [#Serine-glycine
    - Intraperitoneal administration of L654 over 7 weeks to HFD-fed Ldlr−/− mice resulted in hypocholesterolemic effects and significantly attenuated the progression of atherosclerosis. - L654 and other bacterial glycine lipids in feces, liver, and serum were markedly reduced alongside changes in #Bacteroidetes relative abundance in HFD-fed mice.
  • [1.14
    - NOD-like receptor family pyrin domain-containing protein 3 (NLRP3) inflammasome and gut microbiota are closely related to the occurrence and development of AS
  • [1.15] [#Hearth attack] [#Carnitine, #Crotonobetaine, #TMAO, #γ-butyrobetaine] [#Meat-based diet
  • [1.5
    - In a mouse model, it was demonstrated that #Methanobrevibacter smithii, #Methanosarcina mazei, and #Methanomicrococcus blatticola use #TMA as growth substrates, resulting in reduced atherosclerosis
  • [1.16
    - Trimethylamine (#TMA) is generated by the gut microbiome and in the host converted by flavin-containing monooxygenase (FMO3) into trimethylamine N-oxide (#TMAO), which has been implicated in chronic cardiovascular and metabolic diseases. - Using cell culture systems and patient biopsies > #TMAO reprograms skin fibroblasts, vascular endothelial cells, and adipocytic progenitor cells into myofibroblasts via the putative #TMAO receptor protein R-like endoplasmic reticulum kinase (PERK). - FMO3 was detected in skin fibroblasts and its expression stimulated by TGF-β1. - FMO3 was elevated in #Systemic sclerosis skin biopsies and in #Systemic sclerosis fibroblasts.
  • [1.17] [#Human end-stage renal disease
    - #TMAO is a major risk factor for cardiovascular disease, renal fibrosis and functional impairment, atherosclerosis, and #Colorectal cancer.
  • [1.18
    - Depletion of Bacteroides xylanisolvens, Odoribacter splanchnicus, Eubacterium eligens, Roseburia inulinivorans, and Roseburia intestinalis. - At the functional level, healthy metagenomes were both enriched in pathways of starch degradation V, glycolysis III (from glucose), CDP‐diacylglycerol biosynthesis, and folate transformations. - R inulinivorans and R intestinalis are major contributors to starch degradation V. - E eligens greatly contribute to the pathway CDP‐diacylglycerol biosynthesis. - B xylanisolvens and B uniformis contribute to folate transformations II. - Two gut microbial metabolites, nicotinic acid and hydrocinnamic acid, had significantly higher predicted abundance in the control samples compared to the patients in the Chinese cohort, and interestinglynicotinic acid is already an effective lipid‐lowering drug to reducing cardiovascular risk.
  • [1.19
    - The gut microbiota composition of patients with atherosclerosis (AS) contains relatively high levels of Collinsella.

Common References