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Frontiers | A study of the correlation between stroke and gut microbiota over the last 20years: a bibliometric analysis

Purpose: This study intends to uncover a more thorough knowledge structure, research hotspots, and future trends in the field by presenting an overview of the relationship between stroke and gut microbiota in the past two decades. Method: Studies on stroke and gut microbiota correlations published between 1st January 2002 and 31st December 2021 were retrieved from the Web of Science Core Collection and then visualised and scientometrically analysed using CiteSpace V. Results: A total of 660 papers were included in the study, among which the USA, the UK, and Germany were the leading research centres. Cleveland Clinic, Southern Medical University, and Chinese Academy of Science were the top three institutions. The NATURE was the most frequently co-cited journal. STANLEY L HAZEN was the most published author, and Tang WHW was the most cited one. The co-occurrence analysis revealed eight clusters (i.e., brain-gut microbiota axis, fecal microbiome transplantation, gut microbiota, hypertension, TMAO, ischemic stroke, neuroinflammation, atopobiosis). "gut microbiota," "Escherichia coli," "cardiovascular disease," "risk," "disease," "ischemic stroke," "stroke," "metabolism," "inflammation," and "phosphatidylcholine" were the most recent keyword explosions. Conclusions: Findings suggest that in the next ten years, the number of publications produced annually may increase significantly. Future research trends tend to concentrate on the mechanisms of stroke and gut microbiota, with the inflammation and immunological mechanisms, TMAO, and faecal transplantation as hotspots. And the relationship between these mechanisms and a particular cardiovascular illness may also be a future research trend.

Akasaka , Aichi , Japan , Totsuka , Kanagawa , Fukuoka , Atarashi , Nara , United-states , Iran , Ibaraki , Osaka

Frontiers | Contribution of the Gut Microbiota to Intestinal Fibrosis in Crohn's Disease

In Crohn’s disease (CD), intestinal fibrosis is a critical determinant of a patient’s prognosis. Although inflammation may be a prerequisite for the initiation of intestinal fibrosis, research shows that the progression or continuation of intestinal fibrosis can occur independently of inflammation. Thus, once initiated, intestinal fibrosis may persist even if medical treatment controls inflammation. Clearly, an understanding of the pathophysiological mechanisms of intestinal fibrosis is required to diminish its occurrence. Accumulating evidence suggests that the gut microbiota contributes to the pathogenesis of intestinal fibrosis. For example, the presence of antibodies against gut microbes can predict which CD patients will have intestinal complications. In addition, microbial ligands can activate intestinal fibroblasts, thereby inducing the production of extracellular matrix. Moreover, in various animal models, bacterial infection can lead to the development of intestinal fibrosis. In this review, we summarize the current knowledge of the link between intestinal fibrosis in CD and the gut microbiota. We highlight basic science and clinical evidence that the gut microbiota can be causative for intestinal fibrosis in CD and provide valuable information about the animal models used to investigate intestinal fibrosis.

Zeissig , Sachsen , Germany , Japan , United-kingdom , Nakase , Hyogo , Shiokawa , Fukushima , Atarashi , Nara , Setoyama