Gut Microbiota and Atherosclerosis—Focusing on the Plaque Stability

Shen, Xinyi; Li, Lihua; Sun, Zhen; Zang, Guangyao; Zhang, Lili; Shao, Chen; Wang, Zhongqun

doi:10.3389/fcvm.2021.668532

Cited by 49 publications

(41 citation statements)

References 204 publications

(230 reference statements)

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“…The presence of microorganisms in the atheroma plaque is well established, and some studies have shown that the abundance of certain phyla could correlate with plaque stability and overall inflammation [ 346 , 347 ]. For instance, bacterial DNA from pathogenic families, such as Helicobacteraceae or Neisseriaceae , has been shown to be more abundant in plaques of symptomatic patients [ 348 , 349 ]. Nevertheless, these results need to be corroborated in larger studies.…”

Section: Microbiotamentioning

confidence: 99%

Pathophysiology of Atherosclerosis

Jebari-Benslaiman

Galicia-García

Larrea-Sebal

et al. 2022

IJMS

391

208

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Atherosclerosis is the main risk factor for cardiovascular disease (CVD), which is the leading cause of mortality worldwide. Atherosclerosis is initiated by endothelium activation and, followed by a cascade of events (accumulation of lipids, fibrous elements, and calcification), triggers the vessel narrowing and activation of inflammatory pathways. The resultant atheroma plaque, along with these processes, results in cardiovascular complications. This review focuses on the different stages of atherosclerosis development, ranging from endothelial dysfunction to plaque rupture. In addition, the post-transcriptional regulation and modulation of atheroma plaque by microRNAs and lncRNAs, the role of microbiota, and the importance of sex as a crucial risk factor in atherosclerosis are covered here in order to provide a global view of the disease.

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Section: Microbiotamentioning

confidence: 99%

Pathophysiology of Atherosclerosis

Jebari-Benslaiman

Galicia-García

Larrea-Sebal

et al. 2022

IJMS

391

208

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“…These differences may be partially explained by the specific mouse models (high-fat diet versus high-fat diet plus surgical implantation of perivascular carotid collars) or the experimental time lines used [ 18 , 22 ]. Other potential explanations are differences in food compositions or microbiota secondary to the specific animal husbandry conditions [ 54 , 55 ]. Several studies have demonstrated a relationship between microbiota and atherosclerosis [ 54 , 55 ].…”

Section: Discussionmentioning

confidence: 99%

“…Other potential explanations are differences in food compositions or microbiota secondary to the specific animal husbandry conditions [ 54 , 55 ]. Several studies have demonstrated a relationship between microbiota and atherosclerosis [ 54 , 55 ]. Our current data show that changes in the metabolic state (hyperlipidemia versus hyperglycemia) have an impact on plaque stability, supporting that additional factors impact the role of hypercoagulability in atherosclerosis.…”

Section: Discussionmentioning

confidence: 99%

Hypercoagulability Impairs Plaque Stability in Diabetes-Induced Atherosclerosis

et al. 2022

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Diabetes mellitus, which is largely driven by nutritional and behavioral factors, is characterized by accelerated atherosclerosis with impaired plaque stability. Atherosclerosis and associated complications are the major cause of mortality in diabetic patients. Efficient therapeutic concepts for diabetes-associated atherosclerosis are lacking. Atherosclerosis among diabetic patients is associated with reduced endothelial thrombomodulin (TM) expression and impaired activated protein C (aPC) generation. Here, we demonstrate that atherosclerotic plaque stability is reduced in hyperglycemic mice expressing dysfunctional TM (TMPro/Pro mice), which have a pro-coagulant phenotype due to impaired thrombin inhibition and markedly reduced aPC generation. The vessel lumen and plaque size of atherosclerotic lesions in the truncus brachiocephalic were decreased in diabetic TMPro/Pro ApoE-/- mice compared to diabetic ApoE-/- mice. While lipid accumulation in lesions of diabetic TMPro/Pro ApoE-/- mice was lower than that in diabetic ApoE-/- mice, morphometric analyses revealed more prominent signs of instable plaques, such as a larger necrotic core area and decreased fibrous cap thickness in diabetic TMPro/Pro ApoE-/- mice. Congruently, more macrophages and fewer smooth muscle cells were observed within lesions of diabetic TMPro/Pro ApoE-/- mice. Thus, impaired TM function reduces plaque stability, a characteristic of hyperglycemia-associated plaques, thus suggesting the crucial role of impaired TM function in mediating diabetes-associated atherosclerosis.

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“…Gut bacteria of taxa Erysipelotrichia produce TMA following choline metabolization, thus decreasing the bioavailability of this macronutrient and increasing the portal influx of TMA and its conversion to trimethylamine N-oxide (TMAO). This small metabolite [ 642 , 643 , 644 , 645 , 646 , 647 , 648 ] is associated with atherosclerosis and cardiovascular complications, including myocardial infarction and stroke [ 646 , 649 , 650 , 651 , 652 ]. In addition, increased TMAO levels correlate with the presence of type 2 diabetes mellitus, glycemic control in type 2 diabetes mellitus, its complications, and steatogenic effects [ 653 , 654 , 655 , 656 , 657 , 658 , 659 ].…”

Section: Intestinal Barrier Features In Nafldmentioning

confidence: 99%

Intestinal Barrier and Permeability in Health, Obesity and NAFLD

et al. 2021

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The largest surface of the human body exposed to the external environment is the gut. At this level, the intestinal barrier includes luminal microbes, the mucin layer, gastrointestinal motility and secretion, enterocytes, immune cells, gut vascular barrier, and liver barrier. A healthy intestinal barrier is characterized by the selective permeability of nutrients, metabolites, water, and bacterial products, and processes are governed by cellular, neural, immune, and hormonal factors. Disrupted gut permeability (leaky gut syndrome) can represent a predisposing or aggravating condition in obesity and the metabolically associated liver steatosis (nonalcoholic fatty liver disease, NAFLD). In what follows, we describe the morphological-functional features of the intestinal barrier, the role of major modifiers of the intestinal barrier, and discuss the recent evidence pointing to the key role of intestinal permeability in obesity/NAFLD.

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Gut Microbiota and Atherosclerosis—Focusing on the Plaque Stability

Cited by 49 publications

References 204 publications

Pathophysiology of Atherosclerosis

Pathophysiology of Atherosclerosis

Hypercoagulability Impairs Plaque Stability in Diabetes-Induced Atherosclerosis

Intestinal Barrier and Permeability in Health, Obesity and NAFLD

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