空军军医大学武胜昔教授团队的论文发现了环境因素双重打击自闭症模型中H2S的升高是社会缺陷的基础。相关论文发表在2026年3月23日出版的《神经科学通报》杂志上。

考虑到最近有报道称线粒体相关的氨基酸代谢有助于ASD的发展，研究人员探讨了硫化氢（H₂S），一种含硫氨基酸代谢的气体产物，在环境因子双击（DH）诱导的ASD小鼠社会缺陷中的作用。课题组人员检测到DH小鼠前扣带皮层突触和线粒体功能障碍、H₂S升高、含硫代谢物失调以及胱硫氨酸-β-合成酶（CBS）上调。抑制线粒体功能可诱导野生型神经元中H₂S的积累，而引入健康线粒体可抑制DH神经元中H₂S的水平。抑制CBS或限制硫摄入可显著改善DH小鼠的突触功能障碍、社交障碍和焦虑样行为。在人DH神经元和ASD患者中检测到类似的H₂S积累。他们的数据证明了H₂S超载在环境因素诱发的ASD的社交功能障碍中的作用。

研究人员表示，环境因素诱发自闭症谱系障碍（ASD）的潜在机制在很大程度上仍不清楚。

附：英文原文

Title: Elevation of H2S Underlies Social Deficits in Environmental Factor Double-Hit Autism Model

Author: Ma, Hongyu, Xu, Qing, Dong, Songqi, Guo, Mengxin, Liu, Hanze, Wang, Taozhi, Wang, Mengmeng, Wang, Yazhou, Wu, Shengxi

Issue&Volume: 2026-03-23

Abstract: The underlying mechanism for the environmental factor-induced autism spectrum disorder (ASD) remains largely unclear. Considering the recent reports that mitochondria-associated amino acid metabolism contributes to ASD development, we explored the roles of hydrogen sulfide (H2S), a gaseous product of sulfur-containing amino acid metabolism, in the social deficits of ASD mice induced by the environmental factor double-hit (DH). We detected synaptic and mitochondrial dysfunction, elevation of H2S, dysregulation of sulfur-containing metabolites, and upregulation of cystathionine-β-synthase (CBS) in the anterior cingulate cortex of DH mice. Inhibiting mitochondrial function induced H2S accumulation in wild-type neurons, whereas introducing healthy mitochondria suppressed H2S levels in DH neurons. Knocking down CBS or restricting sulfur intake significantly ameliorated synaptic dysfunction, social impairments, and anxiety-like behaviors in DH mice. Similar H2S accumulation was detected in human DH neurons and ASD patients. Our data demonstrated a role of H2S overload in the social dysfunction of environmental factor-induced ASD.

DOI: 10.1007/s12264-026-01608-3

Source: https://link.springer.com/article/10.1007/s12264-026-01608-3