The gut microbe-derived metabolite trimethylamine-N-oxide induces aortic valve fibrosis via PERK/ATF-4 and IRE-1α/XBP-1s signaling in vitro and in vivo

Xiong, Zhenyu; Li, Jiaying; Huang, Rihua; Zhou, Huimin; Xu, Xingfeng; Zhang, Shaozhao; Xie, Peihan; Li, Miaohong; Guo, Yue; Liao, Xinxue; Zhuang, Xiaodong

doi:10.1016/j.atherosclerosis.2023.117431

Cited by 5 publications

(1 citation statement)

References 44 publications

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“…Treatment with 3,3-dimethyl-1-butanol, which inhibits the formation of TMAO, leads to reduced fibrosis. Finally, high-choline and fat diet in treated mice was shown to increase TMAO levels and activation of the aforementioned pathways, thus subsequently leading to increased fibrosis [44].…”

Section: Gm and Vhdmentioning

confidence: 95%

Gut Microbiome and Its Role in Valvular Heart Disease: Not a “Gutted” Relationship

Nayak,

Dimitriadis,

Pyrpyris

et al. 2024

Life

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The role of the gut microbiome (GM) and oral microbiome (OM) in cardiovascular disease (CVD) has been increasingly being understood in recent years. It is well known that GM is a risk factor for various CVD phenotypes, including hypertension, dyslipidemia, heart failure and atrial fibrillation. However, its role in valvular heart disease (VHD) is less well understood. Research shows that, direct, microbe-mediated and indirect, metabolite-mediated damage as a result of gut dysbiosis and environmental factors results in a subclinical, chronic, systemic inflammatory state, which promotes inflammatory cell infiltration in heart valves and subsequently, via pro-inflammatory molecules, initiates a cascade of reaction, resulting in valve calcification, fibrosis and dysfunction. This relationship between GM and VHD adds a pathophysiological link to the pathogenesis of VHD, which can be aimed therapeutically, in order to prevent or regress any risk for valvular pathologies. Therapeutic interventions include dietary modifications and lifestyle interventions, in order to influence environmental factors that can promote gut dysbiosis. Furthermore, the combination of probiotics and prebiotics, as well as fecal m transplantation and targeted treatment with inducers or inhibitors of microbial enzymes have showed promising results in animal and/or clinical studies, with the potential to reduce the inflammatory state and restore the normal gut flora in patients. This review, thus, is going to discuss the pathophysiological links behind the relationship of GM, CVD and VHD, as well as explore the recent data regarding the effect of GM-altering treatment in CVD, cardiac function and systemic inflammation.

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Section: Gm and Vhdmentioning

confidence: 95%

Gut Microbiome and Its Role in Valvular Heart Disease: Not a “Gutted” Relationship

Nayak,

Dimitriadis,

Pyrpyris

et al. 2024

Life

View full text Add to dashboard Cite

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Deficiency of flavin-containing monooxygenase 3 protects kidney function after ischemia–reperfusion in mice

Wang,

Zhang

et al. 2024

Commun Biol

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Research advances in understanding crosstalk between organs and pancreatic β‐cell dysfunction

Huang,

Zhu,

Qin

2024

Diabetes Obesity Metabolism

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Obesity has increased dramatically worldwide. Being overweight or obese can lead to various conditions, including dyslipidaemia, hypertension, glucose intolerance and metabolic syndrome (MetS), which may further lead to type 2 diabetes mellitus (T2DM). Previous studies have identified a link between β‐cell dysfunction and the severity of MetS, with multiple organs and tissues affected. Identifying the associations between pancreatic β‐cell dysfunction and organs is critical. Research has focused on the interaction between the liver, gut and pancreatic β‐cells. However, the mechanisms and related core targets are still not perfectly elucidated. The aims of this review were to summarize the mechanisms of β‐cell dysfunction and to explore the potential pathogenic pathways and targets that connect the liver, gut, adipose tissue, muscle, and brain to pancreatic β‐cell dysfunction.

show abstract

The gut microbe-derived metabolite trimethylamine-N-oxide induces aortic valve fibrosis via PERK/ATF-4 and IRE-1α/XBP-1s signaling in vitro and in vivo

Cited by 5 publications

References 44 publications

Gut Microbiome and Its Role in Valvular Heart Disease: Not a “Gutted” Relationship

Gut Microbiome and Its Role in Valvular Heart Disease: Not a “Gutted” Relationship

Deficiency of flavin-containing monooxygenase 3 protects kidney function after ischemia–reperfusion in mice

Research advances in understanding crosstalk between organs and pancreatic β‐cell dysfunction

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