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肠道微生物失调与心血管疾病之间的桥梁。

Bridging the Gap between Gut Microbial Dysbiosis and Cardiovascular Diseases.

机构信息

Bachelor of Health Sciences (Honours), Faculty of Health Sciences, McMaster University, Hamilton, ON L8S 4L8, Canada.

MD Program, Faculty of Medicine, University of Toronto, Toronto, ON M5S 1A8, Canada.

出版信息

Nutrients. 2017 Aug 10;9(8):859. doi: 10.3390/nu9080859.

Abstract

The human gut is heavily colonized by a community of microbiota, primarily bacteria, that exists in a symbiotic relationship with the host and plays a critical role in maintaining host homeostasis. The consumption of a high-fat (HF) diet has been shown to induce gut dysbiosis and reduce intestinal integrity. Recent studies have revealed that dysbiosis contributes to the progression of cardiovascular diseases (CVDs) by promoting two major CVD risk factors-atherosclerosis and hypertension. Imbalances in host-microbial interaction impair homeostatic mechanisms that regulate health and can activate multiple pathways leading to CVD risk factor progression. Dysbiosis has been implicated in the development of atherosclerosis through metabolism-independent and metabolite-dependent pathways. This review will illustrate how these pathways contribute to the various stages of atherosclerotic plaque progression. In addition, dysbiosis can promote hypertension through vascular fibrosis and an alteration of vascular tone. As CVD is the number one cause of death globally, investigating the gut microbiota as a locus of intervention presents a novel and clinically relevant avenue for future research, with vast therapeutic potential.

摘要

人类肠道被大量的微生物群落定植,主要是细菌,它们与宿主共生,并在维持宿主内稳态方面发挥着关键作用。高脂肪(HF)饮食的摄入已被证明会导致肠道菌群失调并降低肠道完整性。最近的研究表明,菌群失调通过促进两大心血管疾病(CVD)风险因素——动脉粥样硬化和高血压,促进心血管疾病的进展。宿主-微生物相互作用的失衡会破坏调节健康的内稳态机制,并激活导致 CVD 风险因素进展的多种途径。菌群失调通过代谢非依赖性和代谢依赖性途径参与动脉粥样硬化的发生。本综述将说明这些途径如何促进动脉粥样硬化斑块进展的各个阶段。此外,菌群失调可通过血管纤维化和血管张力改变来促进高血压。由于 CVD 是全球头号死因,因此将肠道微生物组作为干预靶点进行研究为未来的研究提供了一个新颖且具有临床相关性的途径,具有巨大的治疗潜力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8e05/5579652/a01a08788d9f/nutrients-09-00859-g001.jpg

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