We can't find the internet
Attempting to reconnect
Something went wrong!
Hang in there while we get back on track
Airborne polystyrene nanoplastics exposure leads to heart failure via ECM-receptor interaction and PI3K/AKT/BCL-2 pathways
AI summary Read the abstract
Mice exposed to airborne polystyrene nanoplastics for just two weeks showed significant heart damage, including reduced heart mass, slowed heart rate, and signs of heart failure. The study suggests that inhaled nanoplastics harm cardiac tissue through specific molecular pathways, raising concerns about the cardiovascular risks of breathing in plastic-contaminated air.
Environmental contamination has been recognized as a significant threat to human well-being, and recent findings of microplastic presence in human cardiac tissues have raised concerns. However, research on the effects of airborne nanoplastics (NPs) on cardiac physiology remains limited. We utilized a comprehensive body exposure apparatus to simulate the impact of airborne polystyrene NPs pollution, focusing on understanding how airborne NPs affect cardiac morphology and function. Following two weeks of NPs exposure, mice exhibited a 23.89 ± 8.30 % reduction in heart mass, a 20.05 ± 2.97 % decrease in heart rate as detected, and a myocardial electrical conduction block. Echocardiography showed significant changes in cardiac contractility, with increases in cardiac ejection fraction and stroke volume of 13.00 ± 3.00 % and 43.00 ± 17.00 %, respectively. In addition, histologic assessments revealed signs of ventricular hypertrophy, ventricular myocardial hypertrophy, and myocardial necrotic fibrosis. Of particular interest, our mechanistic investigations highlighted the harmful effects of NPs on cardiac structure and function, mediated through extracellular matrix (ECM) receptor interactions and the PI3K/AKT/BCL-2 signaling pathway. The insights gained provide a foundation for understanding the risks posed by airborne NPs to human cardiac health, emphasizing the need for increased vigilance and implementation of mitigation strategies in environmental management.
More Papers Like This
Multi-dimensional evaluation of cardiotoxicity in mice following respiratory exposure to polystyrene nanoplastics
AI summary Read the abstract
Researchers exposed mice to polystyrene nanoplastics through inhalation and found that even short-term breathing exposure caused heart damage, including inflammation and weakened heart function. The damage got worse with higher doses and longer exposure times, with energy production in heart cells being disrupted through mitochondrial damage. This is one of the first studies to show that breathing in nanoplastics can directly harm the heart, raising concerns about airborne plastic particle exposure in humans.
Cardiotoxicity of polystyrene nanoplastics and associated mechanism of myocardial cell injury in mice
AI summary Read the abstract
Mice exposed to polystyrene nanoplastics for 42 days developed enlarged hearts, thinner heart walls, and weaker heart contractions in a dose-dependent manner. The nanoplastics triggered inflammation and oxidative stress in heart muscle cells through specific signaling pathways. These findings suggest that nanoplastic exposure could contribute to heart disease, including a condition called dilated cardiomyopathy.
Polystyrene nanoplastics induce cardiotoxicity by upregulating HIPK2 and activating the P53 and TGF-β1/Smad3 pathways
AI summary Read the abstract
Researchers demonstrated that oral exposure to polystyrene nanoplastics in mice causes cardiac fibrosis, cardiomyocyte death, and impaired heart function by upregulating the protein HIPK2 and activating P53 and TGF-β1/Smad3 signaling pathways, with effects worsened in animals with pre-existing heart disease — implicating nanoplastics as a cardiovascular risk factor.
Polystyrene nanoplastics exacerbate lipopolysaccharide-induced myocardial fibrosis and autophagy in mice via ROS/TGF-β1/Smad
AI summary Read the abstract
Researchers found that polystyrene nanoplastics worsened heart damage in mice already exposed to bacterial toxins, accelerating scarring and disrupting normal heart tissue maintenance. The combined exposure triggered increased oxidative stress and activated a specific signaling pathway linked to tissue fibrosis. The study suggests that nanoplastic exposure could amplify existing cardiac stress, potentially compounding heart problems when the body is already under inflammatory challenge.
Micro(nano)plastics in the Development of Myocardial Fibrosis: From Clinical Detection to Molecular Mechanism
AI summary Read the abstract
Researchers found that micro- and nanoplastic burden in human cardiac tissue—particularly nanoplastics—was positively associated with myocardial fibrosis severity, and confirmed in mice that polystyrene nanoplastic exposure worsens stress-induced cardiac remodeling by activating inflammatory, extracellular matrix, and metabolic pathways.
Research digests by email
When a large batch of papers lands in the Atlas, we read through it and send a short write-up of what stood out.