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ORIGINAL RESEARCH article
Front. Cell. Infect. Microbiol.
Sec. Intestinal Microbiome
Volume 15 - 2025 | doi: 10.3389/fcimb.2025.1522431
This article is part of the Research Topic Gut Microbiota-Derived Metabolites and Cardiovascular Diseases View all 5 articles
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Adequate sleep is essential for relieving stress and rejuvenating the mind; however, undesirable physiological and pathological responses resulting from sleep insufficiency or sleep deprivation (SD) are becoming increasingly common. However, the influence of sleep deficiency on gut microbiota and microbiota-associated human diseases, especially on cardiac diseases remain controversial. Here, we constructed the experimental SD model in mice and found it significantly resulted in weakness, depression-like behaviors, and multiple organs dysfunction. Intriguingly, SD mice developed pathogenic cardiac hypertrophy and fibrosis with poor ejection fraction as well as fractional shortening.16s rRNA sequencing demonstrated that SD-induced the pathogenic effects of gut microbiota, which was also observed in mice received by fecal microbe from SD mice in fecal microbiota transplantation (FMT) assays. Next, we investigated the therapeutic effects and underlying mechanisms of oxygen therapy in gut microbiota-associated cardiac fibrosis and dysfunction. The environment of 30% oxygen concentration effectively ameliorated the pathological effects on cardiac function. Transcriptome data also found oxygen therapy targeted several hypoxia-dependent pathways and suppressed cardiac collagen production. In conclusion, these results indicated the importance of sufficient sleep in gut microbiota and may represent a potential therapeutic strategy of oxygen environment exerts protective effects in sleepless sufferings through gut microbiota.
Keywords: Sleep Deprivation, Cardiac dysfunction, Gut Microbiota, Oxygen therapy, hypoxia 2
Received: 04 Nov 2024; Accepted: 13 Feb 2025.
Copyright: © 2025 Cai, Li, Bai, Ding, Liu, Fang, Hou, Zhang, Wang, Wang, Jiang, Xiang, Wu, He, Zhang and Ren. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence:
Zixuan Li, School of Life Sciences, Shanghai University, Shanghai, 200444, China
Jie Bai, Department of Pathogen Biology, Naval Medical University, Shanghai, China
Yue Ding, Department of Pathogen Biology, Naval Medical University, Shanghai, China
Ruisang Liu, Naval Medical Center, Shanghai, China
Liben Fang, Naval Medical Center, Shanghai, China
Dengyong Hou, Naval Medical Center, Shanghai, China
Sheng Zhang, Department of Cardiology, Renji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China
Xiaohui Wang, Department of Pathogen Biology, Naval Medical University, Shanghai, China
Yujia Wang, National Key Laboratory of Immunity & Inflammation, Naval Medical University, Shanghai, China
Yuyu Jiang, Department of Pathogen Biology, Naval Medical University, Shanghai, China
Yan Xiang, Department of Pathogen Biology, Naval Medical University, Shanghai, China
Wenhui Wu, College of Food Science & Technology, Shanghai Ocean University, Shanghai, Beijing Municipality, China
Ying He, Naval Medical Center, Shanghai, China
Yunkai Zhang, Naval Medical Center, Shanghai, China
Xiaomeng Ren, Naval Medical Center, Shanghai, China
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