Cardiac function of colorectal cancer mice is remotely controlled by gut microbiota: regulating serum metabolites and myocardial cytokines.

IF 4.9 Q1 MICROBIOLOGY
Zhan-Kui Gao, Chao-Yuan Fan, Bo-Wen Zhang, Jia-Xin Geng, Xing Han, Dan-Qi Xu, Muhammad Arshad, Hao-Xuan Sun, Jiong-Yi Li, Xiangyuan Jin, Xiao-Qin Mu
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Abstract

Several studies have indicated that the dysregulation of microbial metabolites and the inflammatory environment resulting from microbial dysbiosis may contribute to the occurrence and progression of cardiovascular diseases. Therefore, restoring the disordered gut microbiota in patients with colorectal cancer by fecal microbiota transplantation (FMT) has the potential to reduce the incidence of cardiac disease. In this study, we identified cardiac dysfunction in azomethane and dextran sodium sulfate-induced colorectal cancer mice. Intestinal microbes from healthy mice were transferred to colorectal cancer mice, which vastly reversed the disorder of the gut microbiota and effectively alleviated cardiac dysfunction. Moreover, FMT regulated the expression of serum metabolites such as uridine triphosphate (UTP), tiamulin, andrographolide, and N-Acetyl-D-glucosamine, as well as cytokines like TGF-β, IRF5, and β-MHC in the heart. These findings uncover that the disturbed gut microbiota causes cardiac dysfunction in colorectal cancer mice by modulating the expression of serum metabolites and cytokines, which could be alleviated by treatment with FMT.

结肠直肠癌小鼠的心脏功能是由肠道微生物群远程控制的:调节血清代谢物和心肌细胞因子。
多项研究表明,微生物代谢产物的失调和微生物生态失调导致的炎症环境可能与心血管疾病的发生和发展有关。因此,通过粪便微生物群移植(FMT)恢复结直肠癌患者紊乱的肠道微生物群具有降低心脏病发病率的潜力。在这项研究中,我们发现了氮甲烷和葡聚糖硫酸钠诱导的结直肠癌小鼠心功能障碍。将健康小鼠的肠道微生物转移到结直肠癌小鼠身上,极大地逆转了肠道微生物群的紊乱,并有效地缓解了心功能障碍。此外,FMT还调节了血清代谢物如尿苷三磷酸(UTP)、田田霉素、心莲内酯和n -乙酰- d -葡萄糖胺的表达,以及TGF-β、IRF5、β-MHC等细胞因子在心脏中的表达。这些发现揭示了紊乱的肠道微生物群通过调节血清代谢物和细胞因子的表达而引起结直肠癌小鼠的心功能障碍,而FMT治疗可以缓解这种功能障碍。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
CiteScore
7.20
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0.00%
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审稿时长
13 weeks
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