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REVIEW article
Front. Cell. Neurosci.
Sec. Cellular Neuropathology
Volume 19 - 2025 | doi: 10.3389/fncel.2025.1557746
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Stroke is the second leading cause of death and the third leading cause of disability worldwide, with ischemic stroke (IS) accounting for the vast majority of cases. This paper reviews the latest research on intestinal damage, changes in the gut microbiota, and related therapeutic strategies after IS. Following IS, the integrity of the intestinal mucosal barrier is compromised, leading to increased intestinal permeability. The gut microbiota can translocate to other organs, triggering systemic immune responses that inhibit recovery after IS. Moreover, the composition and proportion of the gut microbiota change after IS. The number of beneficial bacteria decreases, whereas the number of harmful bacteria increases. The production of beneficial metabolites, such as short-chain fatty acids (SCFAs), is reduced, and the levels of harmful metabolites, such as trimethylamine N-oxide (TMAO), increase. Antibiotics after IS not only help prevent infection but also have neuroprotective effects. Although poststroke reperfusion therapy can effectively restore cerebral blood flow, it may also cause intestinal mucosal damage and gastrointestinal dysfunction. Nutritional support after IS can alter the gut microbiota structure and promote neurological recovery. Therefore, individualized treatment for IS patients is crucial. In summary, IS affects not only the brain but the entire body system, especially the gut. Intestinal damage and dysbiosis are critical in IS occurrence, development, and prognosis. By protecting the intestinal mucosa and modulating the structure of the gut microbiota, intestinal damage and related infections can be reduced, improving patient prognosis. Future research is needed to explore therapeutic methods targeting the gut microbiota, providing more comprehensive and effective treatment strategies for IS patients.
Keywords: Gut Microbiota, Intestinal injury, ischemic stroke, individualized therapy, Stroke
Received: 10 Jan 2025; Accepted: 04 Apr 2025.
Copyright: © 2025 Shen, Wang, Li, Kang and Gu. 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:
Xianhui Kang, Department of Anesthesiology, First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, 310016, Zhejiang Province, China
Lijuan Gu, Central Laboratory, Renmin Hospital of Wuhan University, Wuhan, 430060, Hubei Province, China
Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.
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