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The Role and Mechanism of Intestinal Flora in Blood Pressure Regulation and Hypertension Development

失调 机制(生物学) 肠道菌群 微生物群 免疫学 发病机制 粪便细菌疗法 生物 生物信息学 医学 生理学 遗传学 抗生素 艰难梭菌 认识论 哲学
作者
Jing Li,Xinchun Yang,Xin Zhou,Jun Cai
出处
期刊:Antioxidants & Redox Signaling [Mary Ann Liebert]
卷期号:34 (10): 811-830 被引量:33
标识
DOI:10.1089/ars.2020.8104
摘要

Significance: Hypertension (HTN) has a complex etiology that is characterized by genetic and environmental factors. It has become a global health burden leading to cardiovascular diseases and kidney diseases, ultimately progressing to premature death. Accumulating evidence indicated that gut microbiome was associated with metabolic disorders and inflammation, which were closely linked to HTN. Recent Advances: Recent studies using bacterial genomic analysis and fecal microbiota transplantation as well as many lines of seminal evidence demonstrated that aberrant gut microbiome was significantly associated with HTN. The intestinal microbiome of both patients and animals with HTN had decreased bacterial diversity, disordered microbial structure and functions, and altered end products of fermentation. Gut dysbiosis and metabolites of the gut microbiota play an important role in blood pressure (BP) control, and they are therefore responsible for developing HTN. Critical Issues: This study aimed at focusing on the recent advances in understanding the role played by gut bacteria and the mechanisms underlying the pathological milieu that induced elevated BP and led to HTN pathogenesis. Potential intervention strategies targeting the correction of gut dysbiosis to improve HTN development were summarized. Future Directions: Larger numbers of fecal transplants from participants with HTN should be carried out to examine the magnitude of BP changes with the replacement of the gut microbiome. The proposed mechanisms for the gut in regulating BP remain to be verified. Whether intervention strategies using probiotics, dietary interventions, bacteriophages, and fecal transplants are feasible for individuals with HTN remains to be explored. Antioxid. Redox Signal. 34, 811–830.
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