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Integrated Evidence for Lysosomal Dysfunction-Mediated Iron Dysregulation induced by PM2.5 Exposure.

Qiong Zhang1,2, Yuese Yuan1,2, Yuetong Liu1,2

  • 1Department of Toxicology, School of Public Health, Peking University, Beijing 100191, China.

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|February 9, 2026
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Summary

Fine particulate matter (PM2.5) exposure disrupts iron homeostasis, leading to iron deficiency and lung injury. Lysosomal dysfunction is identified as a key mechanism, offering potential therapeutic targets for PM2.5-related lung damage.

Keywords:
1,4-NQ-BCFTLFe2+PM2.5autophagybiomarkerlysosometranscription factor EB

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Area of Science:

  • Environmental Health
  • Toxicology
  • Cell Biology

Background:

  • Ambient fine particulate matter (PM2.5) poses significant risks to human health, particularly affecting the respiratory system.
  • Iron (Fe) homeostasis is crucial for cellular function, and its dysregulation is implicated in various diseases.
  • Understanding the interplay between PM2.5 exposure and Fe metabolism is vital for mitigating adverse health outcomes.

Purpose of the Study:

  • To investigate the role of iron homeostasis disruption in PM2.5-induced lung injury.
  • To elucidate the mechanisms by which PM2.5 affects Fe metabolism and cellular function in the lungs.
  • To identify potential biomarkers and therapeutic targets for PM2.5-related pulmonary damage.

Main Methods:

  • Epidemiological analysis of serum ferritin light chain (FTL) levels in relation to residential PM2.5 concentrations.
  • In vivo studies using a PM2.5 analogue (1,4-NQ-BC) in rat lungs to assess FTL, autophagy, and Fe levels.
  • In vitro studies using RAW264.7 cells to examine the effects of 1,4-NQ-BC on Fe transport, autophagy, and lysosomal function.
  • Investigating the role of lysosomal dysfunction in PM-induced Fe deficiency using transcription factor EB overexpression.

Main Results:

  • Serum FTL levels were positively correlated with PM2.5 concentrations, indicating PM2.5-induced disruption of Fe homeostasis.
  • PM2.5 analogue exposure increased FTL and impaired autophagy flux in rat lungs.
  • In vitro, PM2.5 analogue reduced Fe2+ but increased total Fe, activated autophagy, yet impaired lysosomal function and autophagic flux.
  • Lysosomal dysfunction was identified as a novel mechanism contributing to PM-induced Fe2+ deficiency.

Conclusions:

  • PM2.5 exposure disrupts iron homeostasis, leading to Fe2+ deficiency and contributing to lung injury.
  • Lysosomal damage plays a critical role in PM-induced Fe2+ deficiency.
  • FTL and lysosomal function may serve as sensitive biomarkers and potential therapeutic targets for pulmonary injury associated with PM2.5 exposure.