ArticleParticle and fibre toxicology2013
Inhalation of diesel exhaust does not exacerbate cardiac hypertrophy or heart failure in two mouse models of cardiac hypertrophy.
Article in Particle and fibre toxicology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- Development of coronary dysfunction in adult progeny after maternal engineered nanomaterial inhalation during gestation.Scientific reports · 2021Article
- Distinct Phenotypes Induced by Different Degrees of Transverse Aortic Constriction in C57BL/6N Mice.Frontiers in cardiovascular medicine · 2021Article
- Distinct Phenotypes Induced by Three Degrees of Transverse Aortic Constriction in Mice.Scientific reports · 2019Article
- Ambient fine particulate matter exposure induces reversible cardiac dysfunction and fibrosis in juvenile and older female mice.Particle and fibre toxicology · 2018Article
- FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2017Article
- In Utero Exposure of Hyperlipidemic Mice to Diesel Exhaust: Lack of Effects on Atherosclerosis in Adult Offspring Fed a Regular Chow Diet.Cardiovascular toxicology · 2017Article
- Neonatal Diesel Exhaust Particulate Exposure Does Not Predispose Mice to Adult Cardiac Hypertrophy or Heart Failure.International journal of environmental research and public health · 2016Article
- Exposure to concentrated ambient particulate matter induces reversible increase of heart weight in spontaneously hypertensive rats.Particle and fibre toxicology · 2015Article
- Air pollution and adverse cardiac remodeling: clinical effects and basic mechanisms.Frontiers in physiology · 2015Review
- Article
- In utero and early life exposure to diesel exhaust air pollution increases adult susceptibility to heart failure in mice.Particle and fibre toxicology · 2013Article
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
backgroundStrong associations have been observed between exposure to fine ambient particulate matter (PM2.5) and adverse cardiovascular outcomes. In particular, exposure to traffic related PM2.5 has been associated with increases in left ventricular hypertrophy, a strong risk factor for cardiovascular mortality. As much of traffic related PM2.5 is derived from diesel exhaust (DE), we investigated the effects of chronic DE exposure on cardiac hypertrophy and heart failure in the adult mouse by exposing mice to DE combined with either of two mouse models of cardiac hypertrophy: angiotensin II infusion or pressure overload induced by transverse aortic banding.
methodsWild type male C57BL/6 J mice were either infused with angiotensin II (800 ng/kg/min) via osmotic minipump implanted subcutaneously for 1 month, or underwent transverse aortic banding (27 gauge needle 1 week for observing acute reactions, 26 gauge needle 3 months or 6 months for observing chronic reactions). Vehicle (saline) infusion or sham surgery was used as a control. Shortly after surgery, mice were transferred to our exposure facility and randomly assigned to either diesel exhaust (300 or 400 μg/m(3)) or filtered air exposures. After reaching the end of designated time points, echocardiography was performed to measure heart structure and function. Gravimetric analysis was used to measure the ventricular weight to body weight ratio. We also measured heart rate by telemetry using implanted ambulatory ECG monitors.
resultsBoth angiotensin II and transverse aortic banding promoted cardiac hypertrophy compared to vehicle or sham controls. Transverse aortic banding for six months also promoted heart failure in addition to cardiac hypertrophy. In all cases, DE failed to exacerbate the development of hypertrophy or heart failure when compared to filtered air controls. Prolonged DE exposure also led to a decrease in average heart rate.
conclusionsUp to 6-months of DE exposure had no effect on cardiac hypertrophy and heart function induced by angiotensin II stimulation or pressure overload in adult C57BL/6 J mice. This study highlights the potential importance of particle constituents of ambient PM2.5 to elicit cardiotoxic effects. Further investigations on particle constituents and cardiotoxicity are warranted.
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