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Updated: Dec 24, 2025

Aggravation of Myocardial Ischemia upon Particulate Matter Exposure in Atherosclerosis Animal Model
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Real-Ambient Particulate Matter Exposure-Induced Cardiotoxicity in C57/B6 Mice.

Lianhua Cui1, Limei Shi1, Daochuan Li2

  • 1Department of Toxicology, School of Public Health, Qingdao University, Qingdao, China.

Frontiers in Pharmacology
|April 17, 2020
PubMed
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Real-ambient particulate matter exposure-induced FGFR1 methylation contributes to cardiac dysfunction via lipid metabolism disruption.

The Science of the total environment·2023
This summary is machine-generated.

Particulate matter (PM) exposure harms heart health, with Nrf2 playing a complex role. This study used Nrf2 knockout mice to show PM induces cardiotoxicity, affecting heart function and pathways like MAPK.

Area of Science:

  • Environmental Health
  • Cardiovascular Toxicology
  • Molecular Biology

Background:

  • Particulate matter (PM) exposure is linked to cardiovascular disease, but mechanisms remain unclear.
  • Oxidative stress and the Nrf2 pathway are implicated in PM toxicity.
  • Understanding Nrf2's role is crucial for mitigating PM-induced heart damage.

Purpose of the Study:

  • To investigate real-ambient PM-induced cardiotoxicity in mice.
  • To elucidate the role of the Nrf2 pathway in PM cardiotoxicity.
  • To identify molecular pathways affected by PM exposure and Nrf2 status.

Main Methods:

  • Utilized a Nrf2 knockout mouse model with real-ambient PM exposure.
  • Assessed metal deposition, cardiac function (echocardiography), morphology (histopathology), and oxidative stress (MDA assay).
Keywords:
C57/B6 mousecardiotoxicityindividual ventilated cagesmolecular mechanismparticulate matterreal-life exposure

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  • Employed RNA-seq, qPCR, and Western blotting to analyze gene expression and signaling pathways (MAPK, JAK-STAT, TGF-β1).

    • Main Results:

    • PM exposure increased metal levels (Na, K, Se, Fe) and altered heart function and morphology.
    • Nrf2 knockout partially protected against functional changes but not morphological ones, increasing oxidative stress.
    • PM exposure and/or Nrf2 knockout significantly altered thousands of genes and affected MAPK, JAK-STAT, and TGF-β1 signaling pathways.

    Conclusions:

    • PM exposure induces cardiotoxicity in mice, involving Nrf2.
    • Nrf2 exhibits both protective and detrimental roles in PM-induced cardiac effects.
    • MAPK, JAK-STAT, and TGF-β1 pathways are key mediators of PM cardiotoxicity, modulated by Nrf2.