Cell子刊：空军军医大学武胜昔/王亚周团队揭示自闭症相关社交缺陷新机制

Core Viewpoint - The study identifies mitochondrial dysfunction as a potential mechanism for autism-related social deficits through the elevation of H₂S levels and subsequent sulfhydration of synaptic proteins [3][6]. Group 1: Research Findings - Mitochondrial dysfunction leads to increased H₂S levels, which mediates the sulfhydration of the synaptic protein mGluR5, potentially contributing to social deficits associated with autism [3][6]. - The research focused on the anterior cingulate cortex (ACC) and found that overexpression of cystathionine β-synthase (CBS) in wild-type mice impaired synaptic transmission and social function, while its knockdown effectively restored these functions in two autism mouse models [4][6]. - Significant changes in the sulfhydration of synaptic proteins were observed in Shank3b−/− ACC, confirming excessive sulfhydration of mGluR5 in both autism mouse models [4][6]. Group 2: Implications and Mechanisms - The study suggests that excessive H₂S and the sulfhydration of synaptic proteins may be underlying mechanisms for social function impairments in autism [6][7]. - Reducing the intake of sulfur-containing amino acids improved social dysfunction in Shank3b−/− and Fmr1−/y mice, as well as synaptic defects in corresponding human neurons [4][7].