Scholarlink

<p>Methamphetamine (METH) is an illicit stimulant that is in widespread use worldwide. Repeated intake of METH can lead to addiction and multiple-organ damage, which has become a globalized problem. However, the mechanism of METH toxicity remains unclear. The gut and oral microbiota and their metabolites have an impact on host behavior, metabolism, nutrition, and immune response. The available research find that METH not only disrupts the intestinal microbiota, but also alters the metabolites produced by the intestinal microbiota, such as reducing the levels of short-chain fatty acids (SCFAs), indole derivatives and inosine, and increasing the levels of trimethylamine N-oxide and lipopolysaccharide (LPS). The gut microbiota and their metabolites can participate in mediating METH-induced multi-organ toxicity via the intestinal immune interface and the gut-organ axis, thereby regulating processes such as oxidative stress, inflammatory responses, and mitochondrial damage. Concurrently, therapeutic approaches targeting the affected gut microbiota (including probiotic, microbiota transplantation, SCFAs, and indole derivatives) have also been demonstrated to effectively mitigate damage caused by METH abuse. The objective of this review is to establish a link between METH and the microbiota from the gut and oral cavity, based on the available evidence, to gain insight into the potential bidirectional roles of the gut and oral microbiota in METH addiction and METH-related multi-organ toxicity, and to develop future therapeutic strategies.</p> Graphical Abstract <p>Methamphetamine (METH) mediates multi-organ toxic damage through the "microbe-gut-organ axis." It has been established that microorganisms and their metabolites can regulate the pathophysiological processes of diseases in extra-intestinal organs. METH induces gut dysbiosis, allowing inflammatory factors and bioactive substances to enter the circulatory system and affect distant organs. This ultimately disrupts the immune response, metabolic state, and homeostasis of these organs. Meanwhile, these organs can reciprocally influence the gut, indicating that this regulatory axis is bidirectional.</p> <p></p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Roles of gut and oral microbiota in methamphetamine-induced multi-organ toxicity

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年5月7日

查看全文
  • Jiebin Rong,
  • Jingshen Zhuang,
  • Jialong Xu,
  • Xia Yue,
  • Xuebing Chen

摘要

Methamphetamine (METH) is an illicit stimulant that is in widespread use worldwide. Repeated intake of METH can lead to addiction and multiple-organ damage, which has become a globalized problem. However, the mechanism of METH toxicity remains unclear. The gut and oral microbiota and their metabolites have an impact on host behavior, metabolism, nutrition, and immune response. The available research find that METH not only disrupts the intestinal microbiota, but also alters the metabolites produced by the intestinal microbiota, such as reducing the levels of short-chain fatty acids (SCFAs), indole derivatives and inosine, and increasing the levels of trimethylamine N-oxide and lipopolysaccharide (LPS). The gut microbiota and their metabolites can participate in mediating METH-induced multi-organ toxicity via the intestinal immune interface and the gut-organ axis, thereby regulating processes such as oxidative stress, inflammatory responses, and mitochondrial damage. Concurrently, therapeutic approaches targeting the affected gut microbiota (including probiotic, microbiota transplantation, SCFAs, and indole derivatives) have also been demonstrated to effectively mitigate damage caused by METH abuse. The objective of this review is to establish a link between METH and the microbiota from the gut and oral cavity, based on the available evidence, to gain insight into the potential bidirectional roles of the gut and oral microbiota in METH addiction and METH-related multi-organ toxicity, and to develop future therapeutic strategies.

Graphical Abstract

Methamphetamine (METH) mediates multi-organ toxic damage through the "microbe-gut-organ axis." It has been established that microorganisms and their metabolites can regulate the pathophysiological processes of diseases in extra-intestinal organs. METH induces gut dysbiosis, allowing inflammatory factors and bioactive substances to enter the circulatory system and affect distant organs. This ultimately disrupts the immune response, metabolic state, and homeostasis of these organs. Meanwhile, these organs can reciprocally influence the gut, indicating that this regulatory axis is bidirectional.