Exercise does not ameliorate cardiac dysfunction in obese mice exposed to fine particulate matter

Grimmer, Jacob A.; Tanwar, Vineeta; Youtz, Dane J.; Adelstein, Jeremy M.; Baine, Stephen; Carnes, Cynthia A.; Baer, Lisa A.; Stanford, Kristin I.; Wold, Loren E.

doi:10.1016/j.lfs.2019.116885

Cited by 3 publications

(4 citation statements)

References 40 publications

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“…These results are similar to those seen in a previous study that reported the inability of moderate aerobic exercise to provide anti-inflammatory protection in mice exposed to PM 2.5 (99), which may be linked to expression of heat shock protein 70 kilodalton (HSP70) (99,135). The advantages of moderate exercise on cardiovascular function in obese mice (106,121,144), but not in obese mice exposed to PM 2.5 (57), emphasize the consequential results of PM 2.5 exposure in vulnerable populations. However, the use of a high-fat diet-induced obesity model may be more relevant in substantiating whether fine particulate exposure hinders the ability of exercise to mitigate the detrimental cardiovascular effects in diabetic models, as the ob/ob model may have impaired exercise capacity (57).…”

Section: Cardiac Hemodynamicssupporting

confidence: 89%

“…This suggests the possibility that chronic periods of exposure to PM 2.5 could reduce insulin sensitivity and thus potentiate susceptibility to diabetes mellitus, although inflammation may not be the etiology implicated by this study (16). Particularly concerning is the notion that in obese mice, chronic exposure to PM 2.5 can prevent the beneficial effects of exercise on cardiac function and anti-inflammatory pathways (57). Sedentary mice that were exposed to PM 2.5 presented with increased left ventricular diameter (systolic and diastolic) that was not ameliorated in the exercised group.…”

Section: Cardiac Hemodynamicsmentioning

confidence: 78%

“…The advantages of moderate exercise on cardiovascular function in obese mice (106,121,144), but not in obese mice exposed to PM 2.5 (57), emphasize the consequential results of PM 2.5 exposure in vulnerable populations. However, the use of a high-fat diet-induced obesity model may be more relevant in substantiating whether fine particulate exposure hinders the ability of exercise to mitigate the detrimental cardiovascular effects in diabetic models, as the ob/ob model may have impaired exercise capacity (57).…”

Section: Cardiac Hemodynamicsmentioning

confidence: 98%

“…Sedentary mice that were exposed to PM 2.5 presented with increased left ventricular diameter (systolic and diastolic) that was not ameliorated in the exercised group. Moreover, PM 2.5 exposure enhanced CRP, ICAM-1, and vascular cell adhesion protein 1 (VCAM-1), which were elevated in the PM 2.5 exercised group as well (57). These results are similar to those seen in a previous study that reported the inability of moderate aerobic exercise to provide anti-inflammatory protection in mice exposed to PM 2.5 (99), which may be linked to expression of heat shock protein 70 kilodalton (HSP70) (99,135).…”

Section: Cardiac Hemodynamicsmentioning

confidence: 99%

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Cardiovascular adaptations to particle inhalation exposure: molecular mechanisms of the toxicology

Kunovac

Hathaway

Pinti

et al. 2020

American Journal of Physiology-Heart and Circulatory Physiology

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Ambient air, occupational settings, and the use and distribution of consumer products all serve as conduits for toxicant exposure through inhalation. While the pulmonary system remains a primary target following inhalation exposure, cardiovascular implications are exceptionally culpable for increased morbidity and mortality. The epidemiological evidence for cardiovascular dysfunction resulting from acute or chronic inhalation exposure to particulate matter has been well documented, but the mechanisms driving the resulting disturbances remain elusive. In the current review, we aim to summarize the cellular and molecular mechanisms that are directly linked to cardiovascular health following exposure to a variety of inhaled toxicants. The purpose of this review is to provide a comprehensive overview of the biochemical changes in the cardiovascular system following particle inhalation exposure and to highlight potential biomarkers that exist across multiple exposure paradigms. We attempt to integrate these molecular signatures in an effort to provide direction for future investigations. This review also characterizes how molecular responses are modified in at-risk populations, specifically the impact of environmental exposure during critical windows of development. Maternal exposure to particulate matter during gestation can lead to fetal epigenetic reprogramming, resulting in long-term deficits to the cardiovascular system. In both direct and indirect (gestational) exposures, connecting the biochemical mechanisms with functional deficits outlines pathways that can be targeted for future therapeutic intervention. Ultimately, future investigations integrating "omics" based approaches will better elucidate the mechanisms that are altered by xenobiotic inhalation exposure, identify biomarkers, and guide in clinical decision making.

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Section: Cardiac Hemodynamicssupporting

confidence: 89%

Section: Cardiac Hemodynamicsmentioning

confidence: 78%

Section: Cardiac Hemodynamicsmentioning

confidence: 98%

Section: Cardiac Hemodynamicsmentioning

confidence: 99%

See 2 more Smart Citations

Cardiovascular adaptations to particle inhalation exposure: molecular mechanisms of the toxicology

Kunovac

Hathaway

Pinti

et al. 2020

American Journal of Physiology-Heart and Circulatory Physiology

View full text Add to dashboard Cite

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Oxidative stress pathways of air pollution mediated toxicity: Recent insights

et al. 2020

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Heat-not-burn tobacco products: an emerging threat to cardiovascular health

Fried

Gardner

2020

American Journal of Physiology-Heart and Circulatory Physiology

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Cigarette smoking is at all-time lows globally, but the use of electronic cigarettes has increased profoundly. Recent reports of electronic cigarette or vaping use-associated lung injury may lead individuals to explore novel methods of nicotine consumption, such as heat-not-burn devices. IQOS from Philip Morris, a heat-not-burn device, became available for purchase in the United States in October 2019. Philip Morris claims that 8.8 million people have abandoned traditional cigarettes in favor of IQOS; however, evidence suggests that it may act as a gateway or compliment to cigarette smoking, rather than a replacement. Surveys indicate that 96.3% of Korean IQOS users also smoke cigarettes and 45% of Italian users of IQOS had never smoked cigarettes. In the United States, Canada, and England, susceptibility of youth to trying IQOS was slightly lower than electronic cigarettes, but above cigarette smoking. Heat-not-burn products produce mainstream and second-hand emissions of harmful chemicals including nicotine, particulate matter, benzene, acrolein, and tobacco-specific nitrosamines. The levels of these emissions, despite being less than those of traditional cigarettes, are potentially harmful to cardiovascular health. A study of current smokers showed similar acute effects of heat-not-burn tobacco products and traditional cigarettes on heart rate, blood pressure, and arterial stiffness. Rats exposed to IQOS had similar vascular endothelial function impairment to those exposed to cigarettes. Heat-not-burn aerosol exposure of cultured macrophages elicited increased oxidative stress, although less than that induced by cigarette smoke. Further studies are needed to better understand the cardiovascular effects of heat-not-burn tobacco products.

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Exercise does not ameliorate cardiac dysfunction in obese mice exposed to fine particulate matter

Cited by 3 publications

References 40 publications

Cardiovascular adaptations to particle inhalation exposure: molecular mechanisms of the toxicology

Cardiovascular adaptations to particle inhalation exposure: molecular mechanisms of the toxicology

Oxidative stress pathways of air pollution mediated toxicity: Recent insights

Heat-not-burn tobacco products: an emerging threat to cardiovascular health

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