PM2.5 inducing myocardial fibrosis mediated by Ang II/ERK1/2/TGF-β1 signaling pathway in mice model
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Updated: Nov 12, 2025
Aggravation of Myocardial Ischemia upon Particulate Matter Exposure in Atherosclerosis Animal Model
Published on: December 10, 2021
Xiwen Zang1, Jun Zhao2, Chengzhi Lu3
1Tianjin Medical University, Teda International Cardiovascular Hospital, Tianjin, China.
Objects:
To discuss the influence of PM2.5 on myocardial fibrosis and related mechanism.
Methods:
PM2.5 particles were prepared into different concentrations of solution to drip into the mice's trachea twice each week. The mice were divided into five groups, Blank control group (C group), NS control group (J group), high dose group (G group, 10 mg/kg), medium dose group (Z group, 5 mg/kg), and 1ow dose group (D group, 2.5 mg/kg). After 6 weeks, the myocardial fibrosis was observed by HE and Masson staining. The expression of Ang II, ERK1/2, and TGF-β1 was examined by Western Blotting (WB) and Real time PCR (RT-PCR).
Results:
The higher dose PM2.5 was administrated, the worse the myocardial fibrosis was in PM2.5 groups. The expression of Ang II, ERK1/2, and TGF-β1 was increased in higher dose groups in protein and mRNA level.
Conclusion:
1. PM2.5 induced the cardiac fibrosis. 2. PM2.5 dripped into trachea in mice model activated the expression of Ang II, ERK1/2, and TGF-β1. The activation of renin-angiotensin system (RAS) was suggested to participate in the cardiac fibrosis induced by PM2.5.
Insights
Exposure to fine particulate matter (PM2.5) significantly worsens myocardial fibrosis in mice. This occurs through the activation of the renin-angiotensin system (RAS), involving Ang II, ERK1/2, and TGF-β1.
Area of Science:
- Environmental Health
- Cardiovascular Research
- Toxicology
Background:
- Particulate matter (PM2.5) is a major air pollutant linked to cardiovascular diseases.
- Myocardial fibrosis, a key factor in heart dysfunction, is a growing concern.
- Understanding the mechanisms by which PM2.5 affects the heart is crucial for public health.
Purpose of the Study:
- To investigate the impact of PM2.5 exposure on myocardial fibrosis in a mouse model.
- To elucidate the underlying molecular mechanisms, including the role of the renin-angiotensin system (RAS).
Main Methods:
- Mice were exposed to varying concentrations of PM2.5 via tracheal dripping for six weeks.
- Myocardial fibrosis was assessed using Hematoxylin and Eosin (HE) and Masson trichrome staining.
- Expression levels of Angiotensin II (Ang II), ERK1/2, and Transforming Growth Factor-beta 1 (TGF-β1) were quantified using Western Blotting (WB) and Real-time PCR (RT-PCR).
Main Results:
- PM2.5 exposure led to dose-dependent increases in myocardial fibrosis.
- Elevated protein and mRNA levels of Ang II, ERK1/2, and TGF-β1 were observed in PM2.5-exposed groups.
- Higher PM2.5 concentrations correlated with more severe cardiac fibrosis.
Conclusions:
- PM2.5 exposure is a direct inducer of cardiac fibrosis.
- PM2.5 inhalation activates key components of the RAS, including Ang II, ERK1/2, and TGF-β1.
- The activation of the renin-angiotensin system (RAS) plays a significant role in PM2.5-induced myocardial fibrosis.
