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Redox Biol. 2019 Mar 6;22:101161. doi: 10.1016/j.redox.2019.101161. [Epub ahead of print]

Short term Pm2.5 exposure caused a robust lung inflammation, vascular remodeling, and exacerbated transition from left ventricular failure to right ventricular hypertrophy.

Author information

1
Cardiovascular Department, Shanghai Tenth Renmin Hospital of Tongji University, Shanghai, China.
2
College of Life Science, University of Chinese Academy of Sciences, Beijing 100049, China.
3
Shanxi Provincial People's Hospital, Taiyuan, China.
4
Cardiovascular Division and Lillehei Heart Institute, University of Minnesota Medical School, Minneapolis, MN 55455, USA.
5
College of Life Science, University of Chinese Academy of Sciences, Beijing 100049, China. Electronic address: luzhongbing@ucas.ac.cn.
6
Cardiovascular Department, Shanghai Tenth Renmin Hospital of Tongji University, Shanghai, China. Electronic address: xuyawei@tongji.edu.cn.
7
Cardiovascular Division and Lillehei Heart Institute, University of Minnesota Medical School, Minneapolis, MN 55455, USA. Electronic address: chenx106@umn.edu.

Abstract

Heart failure (HF) is the single largest cause for increased hospitalization after fine particulate matter (PM2.5) exposure. Patients with left HF often progress to right ventricular (RV) failure even with optimal medical care. An increase of PM2.5 of 10 μg per cubic meter was associated with a 76% increase in the risk of death from cardiovascular disease in 4 years' period. However, the role and mechanism of PM2.5 in HF progression are not known. Here we investigated the role of PM2.5 exposure in mice with existing HF mice produced by transverse aortic constriction (TAC). TAC-induced HF caused lung inflammation, vascular remodeling and RV hypertrophy. We found increased PM2.5 profoundly exacerbated lung oxidative stress in mice with existing left HF. To our surprise, PM2.5 exposure had no effect on LV hypertrophy and function, but profoundly exacerbated lung inflammation, vascular remodeling, and RV hypertrophy in mice with existing left HF. These striking findings demonstrate that PM2.5 and/or air pollution is a critical factor for overall HF progression by regulating lung oxidative stress, inflammation and remodeling as well as RV hypertrophy. Improving air quality may save HF patients from a dismal fate.

KEYWORDS:

Air pollution; Heart failure; Inflammation; Oxidative stress; PM2.5; Pulmonary hypertension

PMID:
30861460
DOI:
10.1016/j.redox.2019.101161
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