Gut Microbiota Profile Identifies Transition From Compensated Cardiac Hypertrophy to Heart Failure in Hypertensive Rats
Gut Microbiota Profile Identifies Transition From Compensated Cardiac Hypertrophy to Heart Failure in Hypertensive Rats
复制标题
肠道微生物区系鉴定高血压大鼠从代偿性心肌肥厚到心力衰竭的转变
DOI：
10.1161/hypertensionaha.120.15123
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发表时间：
2020-11-01
期刊：
影响因子：
8.3
通讯作者：
Gomez-Garre, Dulcenombre
中科院分区：
文献类型：
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作者：
Gutierrez-Calabres, Elena;Ortega-Hernandez, Adriana;Gomez-Garre, Dulcenombre
心力衰竭（HF）患者表现出的微循环改变可诱导肠道结构和功能变化，这些变化可能影响正常的肠道微生物群落。同时，肠道微生物群可以影响HF进展中涉及的病理机制。然而，尚不清楚肠道微生物群失调是否可以先于HF中心脏改变的发展，或者它仅仅是一个后果。我们的目的是通过比较自发性高血压心力衰竭和自发性高血压大鼠模型来研究肠道微生物群组成与HF发展之间的潜在关系。通过对16 S核糖体RNA基因进行测序，分析了9月龄和19月龄的自发性高血压心力衰竭、自发性高血压大鼠和血压正常的Wistar京都大鼠的肠道微生物群，并预测了与16 S谱相关的KEGG代谢途径。β多样性，厚壁菌/拟杆菌的比例，分类丰度，和潜在的代谢功能的自发性高血压心力衰竭的自发性高血压大鼠之前（9个月）和之后（19个月）的心脏差异显着不同。与Wistar京都大鼠和自发性高血压大鼠相比，9个月大的自发性高血压心力衰竭显示出Paraprevotella、颤螺菌属、Prevotella 9、粪菌属、粪杆菌属、瘤胃梭菌属6、嗜乳杆菌属、丁酸弧菌属、副舒特氏菌属和副杆菌属的显著增加，而瘤胃梭菌属9、颤杆菌属、瘤胃梭菌属、粘螺菌属、肠单胞菌属和阿克曼氏菌属的减少。其中Akkermansia、Prevotella 9、Paraprevotella和Phascolarctobaterium与心脏结构和功能的改变有关。我们的研究结果表明，在HF的高血压模型中，肠道微生物群的特定变化与HF的发展之间存在关联，并进一步支持干预以恢复肠道微生物群作为预防HF的创新治疗策略。
Microcirculatory alterations displayed by patients with heart failure (HF) induce structural and functional intestinal changes that may affect normal gut microbial community. At the same time, gut microbiota can influence pathological mechanisms implicated in HF progression. However, it is unknown whether gut microbiota dysbiosis can precede the development of cardiac alterations in HF or it is only a mere consequence. Our aim was to investigate the potential relationship between gut microbiota composition and HF development by comparing spontaneously hypertensive heart failure and spontaneously hypertensive rat models. Gut microbiota from spontaneously hypertensive heart failure, spontaneously hypertensive rat, and normotensive Wistar Kyoto rats at 9 and 19 months of age was analyzed by sequencing the 16S ribosomal RNA gene, and KEGG metabolic pathways associated to 16S profiles were predicted. Beta diversity,Firmicutes/Bacteroidetesratio, taxonomic abundances, and potential metabolic functions of gut microbiota were significantly different in spontaneously hypertensive heart failure with respect to spontaneously hypertensive rat before (9 months) and after (19 months) cardiac differences were presented. Nine-month-old spontaneously hypertensive heart failure showed a significant increase in the generaParaprevotella, Oscillospira, Prevotella 9, Faecalitalea, Faecalibacterium, Ruminiclostridium 6, Phascolarctobacterium, Butyrivibrio, Parasutterella, and Parabacteroidescompared with both Wistar Kyoto and spontaneously hypertensive rat, whileRuminiclostridium 9,Oscillibacter,Ruminiclostridium,Mucispirillum, Intestinimonas, andAkkermansiawere diminished. Of them,Akkermansia, Prevotella 9,Paraprevotella, andPhascolarctobateriumwere associated to changes in cardiac structure and function. Our results demonstrate an association between specific changes in gut microbiota and the development of HF in a hypertensive model of HF and further support the intervention to restore gut microbiota as an innovative therapeutic strategy for preventing HF.