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Updated: Feb 3, 2026

Left Atrial Stenosis Induced Pulmonary Venous Arterialization and Group 2 Pulmonary Hypertension in Rat
Published on: November 18, 2018
PM2.5 exposure aggravates left heart failure induced pulmonary hypertension
Jun-Jiang Chen1, Wen-Ming Ma2, Jing-Liang Yuan3
1a School of Medicine , Shandong University , Jinan , China.
Abstract:
Aim: Particulate matter 2.5 (PM2.5) exposure is high risk to cardiovascular diseases. We investigated the influence of PM2.5 exposure on pulmonary arterial hypertension (PAH) murine model induced by left ventricular (LV) failure. Methods: Thirty 10 weeks old C57BL/6 mice were randomised to four groups: sham group, sham + PM2.5 group, TAC group, and TAC + PM2.5 group. Eight weeks post TAC surgery, right ventricular (RV) and lung remodelling (Sirius Red staining and WGA Staining), heart and lung function (EF and RVSBP), and fibrotic genes (TGF-ti mRNA expression and collagen III protein level in lung tissue were measured. Results: Exposure to PM2.5 augments TAC induced PAH as evidenced by decreased EF value and increased RVSBP, RV cardiomyocytes size, RV and lung fibrosis, and upregulated expression of collagen III and TGF-a in comparison to TAC group in lung tissues. Even the LV EF value was deceased from 79.3 ± 3.4% to 63.4 ± 2.1% when sham group exposed to PM2.5, PM2.5 exposure had no effect on RVSBP, RV cardiomyocytes' size, RV weight/tibia length, RV and lung fibrosis, and expression of collagen III and TGF-a in sham surgery mice. Conclusions: Exposure to PM2.5 aggravates deterioration of LV failure induced PAH.
Insights
Particulate matter 2.5 (PM2.5) exposure worsens pulmonary arterial hypertension (PAH) in mice with left ventricular (LV) failure. PM2.5 exacerbates cardiac and lung damage, fibrosis, and cardiovascular dysfunction in this model.
Area of Science:
- Cardiovascular Research
- Environmental Health
- Pulmonary Medicine
Background:
- Particulate matter 2.5 (PM2.5) is a known cardiovascular risk factor.
- Left ventricular (LV) failure can lead to pulmonary arterial hypertension (PAH).
Purpose of the Study:
- To investigate the impact of PM2.5 exposure on a murine model of PAH induced by LV failure.
- To determine if PM2.5 exacerbates cardiac and pulmonary remodeling in this model.
Main Methods:
- C57BL/6 mice were subjected to sham surgery or transverse aortic constriction (TAC) to induce LV failure.
- Mice were exposed to PM2.5 or filtered air.
- Evaluated cardiac and lung function, RV and lung remodeling, and fibrotic markers.
Main Results:
- PM2.5 exposure significantly worsened PAH in TAC mice, indicated by increased right ventricular systolic blood pressure (RVSBP), cardiomyocyte size, and RV/lung fibrosis.
- Upregulated expression of collagen III and TGF-β1 in lung tissue was observed in PM2.5-exposed TAC mice.
- PM2.5 alone did not induce significant cardiac or pulmonary pathology in sham-operated mice.
Conclusions:
- PM2.5 exposure exacerbates the progression of PAH in the setting of LV failure.
- Environmental pollutants like PM2.5 pose a significant threat to cardiovascular health, particularly in individuals with pre-existing heart conditions.
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