109451
论文已发表
注册即可获取德孚的最新动态
IF 收录期刊
- 3.4 Breast Cancer (Dove Med Press)
- 3.2 Clin Epidemiol
- 2.6 Cancer Manag Res
- 2.9 Infect Drug Resist
- 3.7 Clin Interv Aging
- 5.1 Drug Des Dev Ther
- 3.1 Int J Chronic Obstr
- 6.6 Int J Nanomed
- 2.6 Int J Women's Health
- 2.9 Neuropsych Dis Treat
- 2.8 OncoTargets Ther
- 2.0 Patient Prefer Adher
- 2.2 Ther Clin Risk Manag
- 2.5 J Pain Res
- 3.0 Diabet Metab Synd Ob
- 3.2 Psychol Res Behav Ma
- 3.4 Nat Sci Sleep
- 1.8 Pharmgenomics Pers Med
- 2.0 Risk Manag Healthc Policy
- 4.1 J Inflamm Res
- 2.0 Int J Gen Med
- 3.4 J Hepatocell Carcinoma
- 3.0 J Asthma Allergy
- 2.2 Clin Cosmet Investig Dermatol
- 2.4 J Multidiscip Healthc
已发表论文
解读纤维肌痛：肠道与免疫系统相互作用的遗传学见解
Authors Niu M, Li J, Sarafian V , Maes M
Received 31 March 2025
Accepted for publication 10 September 2025
Published 31 October 2025 Volume 2025:18 Pages 5685—5699
DOI https://doi.org/10.2147/JPR.S525610
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 2
Editor who approved publication: Professor Michael A Ueberall
Mengqi Niu,1,2 Jing Li,1,2 Victoria Sarafian,3,4 Michael Maes1– 7
1Sichuan Provincial Center for Mental Health, Sichuan Provincial People’s Hospital, School of Medicine, University of Electronic Science and Technology of China, Chengdu, 610072, People’s Republic of China; 2Key Laboratory of Psychosomatic Medicine, Chinese Academy of Medical Sciences, Chengdu, 610072, People’s Republic of China; 3Department of Psychiatry, Medical University of Plovdiv, Plovdiv, Bulgaria; 4Research Institute at Medical University of Plovdiv, Plovdiv, Bulgaria; 5Research and Innovation Program for the Development of MU – Plovdiv (SRIPD-MUP), Network of Research Higher Schools, Medical University of Plovdiv, Plovdiv, Bulgaria; 6Kyung Hee University, Seoul, Korea; 7Department of Psychiatry, Faculty of Medicine, Chulalongkorn University, and King Chulalongkorn Memorial Hospital, the Thai Red Cross Society, Bangkok, Thailand
Correspondence: Michael Maes, Sichuan Provincial Center for Mental Health, Sichuan Provincial People’s Hospital, School of Medicine, University of Electronic Science and Technology of China, Chengdu, 610072, People’s Republic of China, Tel +86 028 8102 0064, Email michaelmaes@uestc.edu.cn
Background: Fibromyalgia (FM) is a chronic disorder characterized by widespread pain and immune dysregulation. Emerging evidence suggests that gut microbiota and inflammatory proteins may contribute to the development of FM. The aim of this study was to investigate the causal relationships between gut microbiota, inflammatory proteins (cytokines/chemokines), and FM using bidirectional Mendelian randomization (MR) and meta-analysis approaches.
Methods: MR analyses were conducted using genetic data from European populations, employing methods such as MR-IVW, MR-Egger, and MR-weighted median. Reverse MR was also performed, with FM treated as the exposure. A meta-analysis was conducted to consolidate the findings.
Results: Ruminococcus gauvreauii was identified as a risk factor for FM, while Enterorhabdus, Parabacteroides, Butyricicoccus, and Prevotella 9 were found to be protective. Five inflammatory proteins—C-X-C motif chemokine 5 (CXCL5), S100-A12, Leukemia inhibitory factor receptor (LIFR), Monocyte chemoattractant protein 2 (MCP-2/CCL8), and Tumor necrosis factor (TNF-α)—exhibited protective associations, while Natural killer cell receptor 2B4 (NKCR-2B4/CD244) and Interleukin-12 subunit beta (IL-12β) were associated with an increased risk of FM.
Conclusion: This study highlights the role of gut microbiota and inflammatory proteins (cytokines/chemokines) in the pathogenesis of FM. Through Gene Ontology (GO) functional enrichment and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses, the findings suggest their involvement in immune regulation, inflammatory responses, and viral pathways. These findings provide new insights into potential therapeutic targets for modulating gut health and immune responses, opening new avenues for future research and clinical interventions.
Keywords: fibromyalgia, gut microbiota, inflammatory proteins, mendelian randomization study, meta analysis, multi-omics
1Sichuan Provincial Center for Mental Health, Sichuan Provincial People’s Hospital, School of Medicine, University of Electronic Science and Technology of China, Chengdu, 610072, People’s Republic of China; 2Key Laboratory of Psychosomatic Medicine, Chinese Academy of Medical Sciences, Chengdu, 610072, People’s Republic of China; 3Department of Psychiatry, Medical University of Plovdiv, Plovdiv, Bulgaria; 4Research Institute at Medical University of Plovdiv, Plovdiv, Bulgaria; 5Research and Innovation Program for the Development of MU – Plovdiv (SRIPD-MUP), Network of Research Higher Schools, Medical University of Plovdiv, Plovdiv, Bulgaria; 6Kyung Hee University, Seoul, Korea; 7Department of Psychiatry, Faculty of Medicine, Chulalongkorn University, and King Chulalongkorn Memorial Hospital, the Thai Red Cross Society, Bangkok, Thailand
Correspondence: Michael Maes, Sichuan Provincial Center for Mental Health, Sichuan Provincial People’s Hospital, School of Medicine, University of Electronic Science and Technology of China, Chengdu, 610072, People’s Republic of China, Tel +86 028 8102 0064, Email michaelmaes@uestc.edu.cn
Background: Fibromyalgia (FM) is a chronic disorder characterized by widespread pain and immune dysregulation. Emerging evidence suggests that gut microbiota and inflammatory proteins may contribute to the development of FM. The aim of this study was to investigate the causal relationships between gut microbiota, inflammatory proteins (cytokines/chemokines), and FM using bidirectional Mendelian randomization (MR) and meta-analysis approaches.
Methods: MR analyses were conducted using genetic data from European populations, employing methods such as MR-IVW, MR-Egger, and MR-weighted median. Reverse MR was also performed, with FM treated as the exposure. A meta-analysis was conducted to consolidate the findings.
Results: Ruminococcus gauvreauii was identified as a risk factor for FM, while Enterorhabdus, Parabacteroides, Butyricicoccus, and Prevotella 9 were found to be protective. Five inflammatory proteins—C-X-C motif chemokine 5 (CXCL5), S100-A12, Leukemia inhibitory factor receptor (LIFR), Monocyte chemoattractant protein 2 (MCP-2/CCL8), and Tumor necrosis factor (TNF-α)—exhibited protective associations, while Natural killer cell receptor 2B4 (NKCR-2B4/CD244) and Interleukin-12 subunit beta (IL-12β) were associated with an increased risk of FM.
Conclusion: This study highlights the role of gut microbiota and inflammatory proteins (cytokines/chemokines) in the pathogenesis of FM. Through Gene Ontology (GO) functional enrichment and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses, the findings suggest their involvement in immune regulation, inflammatory responses, and viral pathways. These findings provide new insights into potential therapeutic targets for modulating gut health and immune responses, opening new avenues for future research and clinical interventions.
Keywords: fibromyalgia, gut microbiota, inflammatory proteins, mendelian randomization study, meta analysis, multi-omics