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已发表论文
母体免疫激活与神经发育障碍：整合分子、细胞及系统机制
Authors Yong Q , Zhao C, Xia L, Zhu T, Xia K
Received 11 April 2025
Accepted for publication 31 October 2025
Published 24 November 2025 Volume 2025:21 Pages 2575—2594
DOI https://doi.org/10.2147/NDT.S533813
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 5
Editor who approved publication: Professor Taro Kishi
Qi Yong,1,* Chao Zhao,1,* Lu Xia,2 Tengfei Zhu,3,4 Kun Xia3
1The Seventh Affiliated Hospital Hengyang Medical School, University of South China (Hunan Provincial Veterans Administration Hospital), Changsha, Hunan, 410000, People’s Republic of China; 2Hunan Key Laboratory of Medical Genetics, MOE Key Laboratory of Pediatric Rare Diseases, School of Life Sciences, Central South University, Changsha, Hunan, 410083, People’s Republic of China; 3MOE Key Laboratory of Pediatric Rare Diseases, University of South China, Hengyang, Hunan, 421001, People’s Republic of China; 4Department of Critical Care Medicine, Shenzhen Third People’s Hospital, Shenzhen, Guangdong, 518112, People’s Republic of China
*These authors contributed equally to this work
Correspondence: Kun Xia, MOE Key Laboratory of Pediatric Rare Diseases, University of South China, Hengyang, Hunan, 421001, People’s Republic of China, Email xiakun@sklmg.edu.cn Tengfei Zhu, MOE Key Laboratory of Pediatric Rare Diseases, University of South China, Hengyang, Hunan, 421001, People’s Republic of China, Email zhutengfei0793@hotmail.com
Abstract: Neurodevelopmental Disorders (NDDs) represent chronic cerebral dysfunctions arising from gene-environment interactions, encompassing conditions such Autism Spectrum Disorders (ASD) and attention-deficit/hyperactivity disorders (ADHD). Emerging evidence identifies Maternal immune activation (MIA) as a critical environmental risk factor for NDDs. Gestational infections, inflammatory responses, or immune dysregulation elevate maternal-fetal inflammatory mediators, which disrupt neurodevelopmental trajectories via placental-fetal signaling cascades. Preclinical models (rodents, non-human primates) demonstrate that MIA induces characteristic NDD phenotypes—including social deficits and cognitive impairments—through microglial hyperactivation, aberrant synaptic pruning, oxidative stress, and mitochondrial dysfunction. Concurrently, gut microbiota dysbiosis and Th17/Treg immune imbalance exacerbate neuroinflammatory processes. Novel therapeutic strategies targeting inflammatory pathways microglial modulation, or microbial homeostasis restoration show translational promise. Future investigations must unravel MIA’s molecular underpinnings and multifactorial interactions to enable early-risk stratification and precision interventions for NDDs.
Keywords: MIA, NDD, Microglia
1The Seventh Affiliated Hospital Hengyang Medical School, University of South China (Hunan Provincial Veterans Administration Hospital), Changsha, Hunan, 410000, People’s Republic of China; 2Hunan Key Laboratory of Medical Genetics, MOE Key Laboratory of Pediatric Rare Diseases, School of Life Sciences, Central South University, Changsha, Hunan, 410083, People’s Republic of China; 3MOE Key Laboratory of Pediatric Rare Diseases, University of South China, Hengyang, Hunan, 421001, People’s Republic of China; 4Department of Critical Care Medicine, Shenzhen Third People’s Hospital, Shenzhen, Guangdong, 518112, People’s Republic of China
*These authors contributed equally to this work
Correspondence: Kun Xia, MOE Key Laboratory of Pediatric Rare Diseases, University of South China, Hengyang, Hunan, 421001, People’s Republic of China, Email xiakun@sklmg.edu.cn Tengfei Zhu, MOE Key Laboratory of Pediatric Rare Diseases, University of South China, Hengyang, Hunan, 421001, People’s Republic of China, Email zhutengfei0793@hotmail.com
Abstract: Neurodevelopmental Disorders (NDDs) represent chronic cerebral dysfunctions arising from gene-environment interactions, encompassing conditions such Autism Spectrum Disorders (ASD) and attention-deficit/hyperactivity disorders (ADHD). Emerging evidence identifies Maternal immune activation (MIA) as a critical environmental risk factor for NDDs. Gestational infections, inflammatory responses, or immune dysregulation elevate maternal-fetal inflammatory mediators, which disrupt neurodevelopmental trajectories via placental-fetal signaling cascades. Preclinical models (rodents, non-human primates) demonstrate that MIA induces characteristic NDD phenotypes—including social deficits and cognitive impairments—through microglial hyperactivation, aberrant synaptic pruning, oxidative stress, and mitochondrial dysfunction. Concurrently, gut microbiota dysbiosis and Th17/Treg immune imbalance exacerbate neuroinflammatory processes. Novel therapeutic strategies targeting inflammatory pathways microglial modulation, or microbial homeostasis restoration show translational promise. Future investigations must unravel MIA’s molecular underpinnings and multifactorial interactions to enable early-risk stratification and precision interventions for NDDs.
Keywords: MIA, NDD, Microglia