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<p>Apurinic/apyrimidinic endonuclease 1 (APE1) is a multifunctional protein that occupies a key position at the interface between base excision repair (BER) and cellular redox control during inflammation. As the major AP endonuclease in the BER pathway, APE1 maintains the genomic stability by the repairing oxidative DNA lesions that accumulate in chronically inflamed tissues. In addition, its redox effector factor 1 (Ref-1) activity modulates a broad range of transcription factors, thereby influencing inflammatory cytokine production and the cellular response to redox imbalance. Through this combination of DNA repair and redox-signaling functions, APE1 acts as a central hub that couples oxidative DNA damage to inflammatory signaling networks. Dysregulation of APE1 expression or subcellular distribution has been associated with various inflammation-associated diseases, reflecting its broad impact on inflammatory pathology. This review summarizes current understanding of APE1’s dual role in inflammation, highlights opportunities and challenges for therapeutic targeting, and discusses its emerging value in the precision monitoring and management of inflammation‑associated diseases.</p>

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Targeting the APE1 hub: integrating DNA repair and redox signaling for precision management of inflammation-associated diseases

  • 期刊论文

  • 发表日期：

    2026年5月7日

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  • Peilan Xu,
  • Peng Zhou,
  • Jia Luo,
  • Yun Liu,
  • He Xiao,
  • Jia Du,
  • Mengxia Li,
  • Chuan Chen

摘要

Apurinic/apyrimidinic endonuclease 1 (APE1) is a multifunctional protein that occupies a key position at the interface between base excision repair (BER) and cellular redox control during inflammation. As the major AP endonuclease in the BER pathway, APE1 maintains the genomic stability by the repairing oxidative DNA lesions that accumulate in chronically inflamed tissues. In addition, its redox effector factor 1 (Ref-1) activity modulates a broad range of transcription factors, thereby influencing inflammatory cytokine production and the cellular response to redox imbalance. Through this combination of DNA repair and redox-signaling functions, APE1 acts as a central hub that couples oxidative DNA damage to inflammatory signaling networks. Dysregulation of APE1 expression or subcellular distribution has been associated with various inflammation-associated diseases, reflecting its broad impact on inflammatory pathology. This review summarizes current understanding of APE1’s dual role in inflammation, highlights opportunities and challenges for therapeutic targeting, and discusses its emerging value in the precision monitoring and management of inflammation‑associated diseases.