Supplemental Digital Content is available in the text. 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/Bacteroidetes ratio, 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 genera Paraprevotella, Oscillospira, Prevotella 9, Faecalitalea, Faecalibacterium, Ruminiclostridium 6, Phascolarctobacterium, Butyrivibrio, Parasutterella, and Parabacteroides compared with both Wistar Kyoto and spontaneously hypertensive rat, while Ruminiclostridium 9, Oscillibacter, Ruminiclostridium, Mucispirillum, Intestinimonas, and Akkermansia were diminished. Of them, Akkermansia, Prevotella 9, Paraprevotella, and Phascolarctobaterium were 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.

中文翻译：

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肠道微生物群谱识别高血压大鼠从代偿性心脏肥大到心力衰竭的转变

补充数字内容在文本中可用。心力衰竭 (HF) 患者表现出的微循环改变会导致肠道结构和功能发生变化，这可能会影响正常的肠道微生物群落。同时，肠道微生物群可以影响与 HF 进展有关的病理机制。然而，尚不清楚肠道微生物群失调是否会先于 HF 心脏改变的发展，或者这仅仅是结果。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。自发性高血压性心力衰竭、自发性高血压大鼠、通过对 16S 核糖体 RNA 基因进行测序，对 9 个月和 19 个月大的血压正常的 Wistar 京都大鼠进行了分析，并预测了与 16S 谱相关的 KEGG 代谢途径。与自发性高血压大鼠相比，β 多样性、厚壁菌门 / 拟杆菌门比、分类丰度和肠道微生物群的潜在代谢功能在自发性高血压心力衰竭中显着不同，在出现心脏差异之前（9 个月）和之后（19 个月）。与 Wistar Kyoto 和自发性高血压大鼠相比，9 个月大的自发性高血压性心力衰竭显示副普雷沃氏菌属、Oscillospira、普氏菌属 9、粪菌属、粪杆菌属、瘤胃梭菌属 6、Phascolarctobacterium、Butyrivibrio、Parasutterella 和 Parabacteroides 属显着增加 而瘤胃梭菌 9、Oscillibacter、瘤胃梭菌、粘螺旋菌、肠单胞菌和阿克曼菌减少。其中，Akkermansia、Prevotella 9、Paraprevotella 和 Phascolarctobaterium 与心脏结构和功能的变化有关。我们的研究结果表明，在 HF 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，并进一步支持将恢复肠道微生物群的干预措施作为预防 HF 的创新治疗策略。