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<p>ALI and ARDS are among the most common diseases in intensive care units, and are characterized by rapid onset and high mortality rates. Dysregulation of macrophage homeostasis is closely associated with the inflammatory cascade in ALI/ARDS. Transcription factors play critical roles in maintaining macrophage immune function. However, the mechanisms by which transcription factors and macrophages regulate the inflammatory imbalance in ALI/ARDS remain largely undefined. Here, we illustrate the role of DDIT3 in regulating macrophage immune function. Our comprehensive bioinformatics analysis revealed that DDIT3 is a key transcriptional regulator of ARDS with superior diagnostic potential. DDIT3 is highly expressed in macrophages and promotes M1 macrophage activation in ARDS patients, and in vivo/vitro models of ALI. DDIT3 deficiency significantly reduces the proportion of M1 macrophages and notably decreases in the secretion of inflammatory cytokines. RNA-seq and CUT&amp;Tag analyses identified KLF10 as a target gene of DDIT3. Moreover, we demonstrated that the inhibition of KLF10 activity reversed the anti-inflammatory effect of DDIT3 silencing by restoring M1 macrophage polarization and inflammatory cytokine secretion. Our findings confirm that DDIT3 is a key regulator of macrophage polarization and inflammatory mediator secretion, suggesting that DDIT3 is a potential therapeutic target for ALI/ARDS.</p>

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The Transcription Factor DDIT3 Regulates Macrophage Function by Inhibiting KLF10 to Attenuate ALI/ARDS Inflammation

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年1月24日

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  • Mengfei Sun,
  • Qianqian Yang,
  • Yingshuai Tan,
  • Chunling Hu,
  • Shilong Zhao,
  • Xiaoxiao Lu,
  • Jing Gao,
  • Lihua Xing

摘要

ALI and ARDS are among the most common diseases in intensive care units, and are characterized by rapid onset and high mortality rates. Dysregulation of macrophage homeostasis is closely associated with the inflammatory cascade in ALI/ARDS. Transcription factors play critical roles in maintaining macrophage immune function. However, the mechanisms by which transcription factors and macrophages regulate the inflammatory imbalance in ALI/ARDS remain largely undefined. Here, we illustrate the role of DDIT3 in regulating macrophage immune function. Our comprehensive bioinformatics analysis revealed that DDIT3 is a key transcriptional regulator of ARDS with superior diagnostic potential. DDIT3 is highly expressed in macrophages and promotes M1 macrophage activation in ARDS patients, and in vivo/vitro models of ALI. DDIT3 deficiency significantly reduces the proportion of M1 macrophages and notably decreases in the secretion of inflammatory cytokines. RNA-seq and CUT&Tag analyses identified KLF10 as a target gene of DDIT3. Moreover, we demonstrated that the inhibition of KLF10 activity reversed the anti-inflammatory effect of DDIT3 silencing by restoring M1 macrophage polarization and inflammatory cytokine secretion. Our findings confirm that DDIT3 is a key regulator of macrophage polarization and inflammatory mediator secretion, suggesting that DDIT3 is a potential therapeutic target for ALI/ARDS.