Frontiers in molecular neuroscience · 2026
Transcriptomic signatures of the insular cortex in a mouse model of neuropathic pain.
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Bai Yang, Yao Guo-Quan, Jiang Cheng-Guo, Zhang Chong, Diao Yu-Gang, Feng Si-Zhe, Liang Guo-Biao, Qiu Xin-Tong, Jiang Wei
Аннотация
BACKGROUND: Neuropathic pain (NP) remains poorly managed by current therapies. Although the insular cortex (IC) is critical for cortical pain processing, a comprehensive spatiotemporal molecular characterization of the IC in NP is lacking.
METHODS: We employed RNA sequencing of the anterior (aIC) and posterior (pIC) insular cortices at 2 and 4 weeks following spared nerve injury in mice. Integrative bioinformatics analyses-including differential expression, functional enrichment, weighted gene co-expression network analysis, and protein-protein interaction (PPI) network construction-were used to delineate the molecular landscape.
RESULTS: Widespread transcriptional dysregulation in the IC was observed, with the number of differentially expressed genes increasing over time. Functional analyses reaffirmed involvement of neuroinflammation and synaptic plasticity-related pathways and further identified dysregulation of mitochondrial pathways-mechanisms commonly implicated in neurodegenerative disorders. Subregion analysis revealed that the aIC exhibited broader and more persistent pathway alterations than the pIC, including programmed cell death (early phase), mitochondrial dysfunction/neurodegeneration (late phase), indicating a progressive stress response unique to the aIC. PPI network analysis identified stage-specific hub genes: early-phase interferon-stimulated genes predominated in both subregions; late-phase hub genes included circadian rhythm regulators, ER stress markers and inflammatory mediators.
CONCLUSION: This study presents a detailed transcriptomic profile of the IC in NP, revealing region- and time-dependent remodeling. Our results confirm known mechanisms and uncover dysregulation reminiscent of neurodegenerative disorders-predominantly in the aIC, suggesting its heightened susceptibility to pain-induced pathology. These findings expand our understanding of IC-mediated pathophysiological processes in NP and may provide a framework for identifying novel therapeutic targets for chronic pain.
METHODS: We employed RNA sequencing of the anterior (aIC) and posterior (pIC) insular cortices at 2 and 4 weeks following spared nerve injury in mice. Integrative bioinformatics analyses-including differential expression, functional enrichment, weighted gene co-expression network analysis, and protein-protein interaction (PPI) network construction-were used to delineate the molecular landscape.
RESULTS: Widespread transcriptional dysregulation in the IC was observed, with the number of differentially expressed genes increasing over time. Functional analyses reaffirmed involvement of neuroinflammation and synaptic plasticity-related pathways and further identified dysregulation of mitochondrial pathways-mechanisms commonly implicated in neurodegenerative disorders. Subregion analysis revealed that the aIC exhibited broader and more persistent pathway alterations than the pIC, including programmed cell death (early phase), mitochondrial dysfunction/neurodegeneration (late phase), indicating a progressive stress response unique to the aIC. PPI network analysis identified stage-specific hub genes: early-phase interferon-stimulated genes predominated in both subregions; late-phase hub genes included circadian rhythm regulators, ER stress markers and inflammatory mediators.
CONCLUSION: This study presents a detailed transcriptomic profile of the IC in NP, revealing region- and time-dependent remodeling. Our results confirm known mechanisms and uncover dysregulation reminiscent of neurodegenerative disorders-predominantly in the aIC, suggesting its heightened susceptibility to pain-induced pathology. These findings expand our understanding of IC-mediated pathophysiological processes in NP and may provide a framework for identifying novel therapeutic targets for chronic pain.