Wang Yi, Lai Han, Zhang Tian, Wu Jing, Tang Huiling, Liang Xuanwei, Ren Dandan, Huang Jinzhu, Li Weihong
Basic Medical College, Chengdu University of Traditional Chinese Medicine, Chengdu, Sichuan Province 610000, PR China.
School of Foreign Languages, Chengdu University of Traditional Chinese Medicine, Chengdu, Sichuan Province 610000, PR China.
Neurosci Biobehav Rev. 2023 Oct;153:105403. doi: 10.1016/j.neubiorev.2023.105403. Epub 2023 Sep 22.
The role of gut dysbiosis in depression is well established. However, recent studies have shown that gut microbiota is regulated by intestinal epithelial cell (IEC) mitochondria, which has yet to receive much attention. This review summarizes the recent developments about the critical role of IEC mitochondria in actively maintaining gut microbiota, intestinal metabolism, and immune homeostasis. We propose that IEC mitochondrial dysfunction alters gut microbiota composition, participates in cell fate, mediates oxidative stress, activates the peripheral immune system, causes peripheral inflammation, and transmits peripheral signals through the vagus and enteric nervous systems. These pathological alterations lead to brain inflammation, disruption of the blood-brain barrier, activation of the hypothalamic-pituitary-adrenal axis, activation of microglia and astrocytes, induction of neuronal loss, and ultimately depression. Furthermore, we highlight the prospect of treating depression through the mitochondria of IECs. These new findings suggest that the mitochondria of IECs may be a newly found important factor in the pathogenesis of depression and represent a potential new strategy for treating depression.
肠道微生物群失调在抑郁症中的作用已得到充分证实。然而,最近的研究表明,肠道微生物群受肠上皮细胞(IEC)线粒体的调节,这一点尚未受到太多关注。本综述总结了IEC线粒体在积极维持肠道微生物群、肠道代谢和免疫稳态方面的关键作用的最新进展。我们提出,IEC线粒体功能障碍会改变肠道微生物群组成,参与细胞命运,介导氧化应激,激活外周免疫系统,引发外周炎症,并通过迷走神经和肠神经系统传递外周信号。这些病理改变会导致脑部炎症、血脑屏障破坏、下丘脑-垂体-肾上腺轴激活、小胶质细胞和星形胶质细胞激活、神经元丢失诱导,最终导致抑郁症。此外,我们强调了通过IEC线粒体治疗抑郁症的前景。这些新发现表明,IEC线粒体可能是抑郁症发病机制中新发现的重要因素,代表了一种潜在的抑郁症治疗新策略。