Vitamin B12 and gut-brain homeostasis in the pathophysiology of ischemic stroke.
Vitamin B12 and gut-brain homeostasis in the pathophysiology of ischemic stroke.
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DOI：
10.1016/j.ebiom.2021.103676
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发表时间：
2021-11
期刊：
影响因子：
11.1
通讯作者：
Mohamadzadeh M
中科院分区：
文献类型：
--
作者：
Roth W;Mohamadzadeh M
中风是世界范围内发病率和死亡率的主要原因。它给病人及其亲人造成了无法估量的痛苦，并带来了巨大的社会代价。减轻中风影响的努力集中在确定预防和治疗的治疗靶点上。肠道微生物组代表了这样一个潜在的目标，因为它对已知导致和恶化中风严重程度的疾病有多方面的影响。维生素B12（VB12）是两种酶的辅助因子，甲基丙二酰辅酶A合酶和甲硫氨酸合酶，对甲硫氨酸和核苷酸的生物合成至关重要。维生素B12缺乏导致代谢底物的积累，如同型半胱氨酸，改变免疫稳态并导致动脉粥样硬化疾病，包括缺血性中风。除了支持细胞功能外，VB12还作为肠道微生物的代谢辅因子。通过塑造微生物群落，VB12进一步影响局部和外周免疫。越来越多的证据表明，由VB12缺乏诱导的肠道生态失调相关的免疫功能障碍可能潜在地导致卒中发病机制、其严重程度和患者结局。在这篇综述中，我们讨论了VB12，肠道微生物和相关代谢产物的复杂相互作用，以及整个缺血性中风的自然史中的免疫稳态。
Stroke is a leading cause of morbidity and mortality worldwide. It inflicts immeasurable suffering on patients and their loved ones and carries an immense social cost. Efforts to mitigate the impact of stroke have focused on identifying therapeutic targets for the prevention and treatment. The gut microbiome represents one such potential target given its multifaceted effects on conditions known to cause and worsen the severity of stroke. Vitamin B12 (VB12) serves as a cofactor for two enzymes, methylmalonyl-CoA synthase and methionine synthase, vital for methionine and nucleotide biosynthesis. VB12 deficiency results in a buildup of metabolic substrates, such as homocysteine, that alter immune homeostasis and contribute to atherosclerotic disorders, including ischemic stroke. In addition to its support of cellular function, VB12 serves as a metabolic cofactor for gut microbes. By shaping microbial communities, VB12 further impacts local and peripheral immunity. Growing evidence suggests that gut dysbiosis-related immune dysfunction induced by VB12 deficiency may potentially contributes to stroke pathogenesis, its severity, and patient outcomes. In this review, we discuss the complex interactions of VB12, gut microbes and the associated metabolites, and immune homeostasis throughout the natural history of ischemic stroke.
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