ArticleNeurochemical research2026
Targeting the YY1/HDAC2 Transcriptional Axis by Neferine Ameliorates Sleep Deprivation-Induced Cognitive Deficits.
Article in Neurochemical research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Epigenetic dysregulation, particularly through histone acetylation dynamics, is critically implicated in sleep deprivation-induced cognitive dysfunction pathogenesis. This study delineates a novel regulatory axis wherein histone deacetylase 2 (HDAC2) deficiency mitigates cognitive deficits, while its upstream transcriptional control mechanisms remain poorly characterized. Through integrative bioinformatics and functional genomics, we identified Yin Yang 1 (YY1) as a direct transcriptional activator of HDAC2. Mechanistic investigations revealed YY1 binds the HDAC2 promoter, enhancing its transcriptional activity. Prefrontal cortical YY1 knockdown in murine models precipitated molecular and neurocognitive improvement, including HDAC2 downregulation, elevated expression of synaptic markers, alongside elevated dendritic spine complexity. These findings position YY1 as a sleep deprivation-responsive epigenetic modulator with intrinsic neuroprotective functionality. Translating these mechanistic insights, we conducted pharmacological screening to identify YY1-reducing therapeutics. Neferine (NEF) emerged as a lead compound, demonstrating dual inhibition of the YY1/HDAC2 axis. In chronic sleep deprivation models, NEF administration rescued synaptic deficits and ameliorated cognitive impairments. Crucially, NEF’s neuroprotective efficacy proved entirely contingent upon intact YY1/HDAC2 signaling, as evidenced by its null effects in HDAC2 conditional knockout models. This study reveals YY1 as a key regulator of HDAC2, identifying the YY1/HDAC2 pathway as a potential therapeutic target for sleep deprivation-induced cognitive deficits.
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