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<p>Chronic inflammatory pain, involving peripheral and central sensitization, and comorbid anxiety symptoms, imposes substantial clinical burdens due to inadequate therapies and unclear molecular mechanisms. This study investigated transcriptomic alterations in dorsal root ganglia (DRG), spinal cord (SC), and anterior cingulate cortex (ACC) following complete Freund’s adjuvant (CFA) administration. RNA-seq revealed distinct long non-coding RNA (lncRNA) and mRNA expression profiles across neural regions. Differentially expressed genes (DEGs) associated with pain-anxiety comorbidity were enriched in pathways related to neuroinflammation, apoptotic regulation, and oxidative stress responses. Functional analyses identified MAPK signaling, chromatin remodeling, and phosphorylation as pivotal biological processes. Comparative transcriptomic profiling further revealed both region-specific and conserved transcriptional signatures. Collectively, our findings elucidate coordinated peripheral-central transcriptional reprogramming during inflammatory pain progression, underscoring the interplay among neuroinflammation, apoptosis, and oxidative stress as central pathogenic mechanisms. The identified DEGs thus constitute promising therapeutic targets for managing chronic inflammatory pain.</p>

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RNA profiling of the dorsal root ganglia, spinal cord, and anterior cingulate cortex in mice with CFA-induced inflammatory pain

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年7月3日

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  • Jiayi Chen,
  • Qingsheng Meng,
  • Yidi Zhao,
  • Canyang Xu,
  • Xuanxiao Wang,
  • Sijia Zhu,
  • Wencai Liu,
  • Kaitai Yang,
  • Tianen Si,
  • Mingrui Li,
  • Songxue Su,
  • Cui Li

摘要

Chronic inflammatory pain, involving peripheral and central sensitization, and comorbid anxiety symptoms, imposes substantial clinical burdens due to inadequate therapies and unclear molecular mechanisms. This study investigated transcriptomic alterations in dorsal root ganglia (DRG), spinal cord (SC), and anterior cingulate cortex (ACC) following complete Freund’s adjuvant (CFA) administration. RNA-seq revealed distinct long non-coding RNA (lncRNA) and mRNA expression profiles across neural regions. Differentially expressed genes (DEGs) associated with pain-anxiety comorbidity were enriched in pathways related to neuroinflammation, apoptotic regulation, and oxidative stress responses. Functional analyses identified MAPK signaling, chromatin remodeling, and phosphorylation as pivotal biological processes. Comparative transcriptomic profiling further revealed both region-specific and conserved transcriptional signatures. Collectively, our findings elucidate coordinated peripheral-central transcriptional reprogramming during inflammatory pain progression, underscoring the interplay among neuroinflammation, apoptosis, and oxidative stress as central pathogenic mechanisms. The identified DEGs thus constitute promising therapeutic targets for managing chronic inflammatory pain.