We can't find the internet
Attempting to reconnect
Something went wrong!
Hang in there while we get back on track
Ferroptosis involved in inhaled polystyrene microplastics leaded myocardial fibrosis through HIF-ROS-SLC7A11/GPX4 Pathway
AI summary Read the abstract
Researchers found that inhaling polystyrene microplastics caused heart muscle scarring (fibrosis) in mice through a process called ferroptosis, a type of iron-dependent cell death. The microplastics triggered a chain reaction involving low oxygen signals and oxidative stress that depleted the heart cells' protective antioxidant systems. This study reveals a specific mechanism by which breathing in airborne microplastics could lead to lasting heart damage.
The issue of microplastic (MPs) pollution has received increased attention in recent years. Studies have indicated that inhalation of microplastics may result in the cardiovascular harm. However, the specific mechanism remains to be elucidated. In this study, 5 µm polystyrene microplastics (PS-MPs) were employed to construct in vivo and in vitro exposure models to investigate the potential mechanisms of microplastic-induced cardiac fibrosis. In vivo model of respiratory exposure to MPs, echocardiography observed a decrease in systolic-diastolic function of the mouse heart, and myocardial tissue showed significant mitochondrial morphological abnormalities and myocardial fibrosis. In vitro models also revealed upregulation of fibrosis indicators in human cardiomyocytes AC16 cells. Transcriptome and RT-qPCR assay exposed that ferroptosis-related pathways were significantly gathered in the MPs group, with decreased expression of ferroptosis related genes SLC7A11 and GPX4. Liproxstatin-1 (Lip-1), a ferroptosis inhibitor, significantly ameliorated MPs-induced cardiomyocyte fibrosis and ferroptosis. We further demonstrated that inhibition of hypoxia-inducible factor α (HIF-α) and oxidative stress ameliorated PS-MPs-induced cardiomyocyte ferroptosis, and thus upregulation of the HIF pathway and oxidative stress may be the upstream mechanism of MPs-induced ferroptosis in myocardial fibrosis. Above all, our study demonstrated that MPs exposure resulted in cardiac fibrosis via the HIF-ROS-SLC7A11/GPX4 signaling pathway.
More Papers Like This
Polystyrene microplastics induce pulmonary fibrosis by promoting alveolar epithelial cell ferroptosis through cGAS/STING signaling
AI summary Read the abstract
Researchers found that mice exposed to polystyrene microplastics through their noses developed lung scarring (fibrosis) because the plastic particles triggered a form of cell death called ferroptosis, involving iron buildup and cell damage in lung tissue. Blocking the specific signaling pathway responsible (cGAS/STING) reduced the lung damage, pointing to a potential treatment approach if microplastic-related lung disease becomes a clinical concern.
Exposure of polystyrene nanoplastics led to ferroptosis on cardiomyocytes
AI summary Read the abstract
Researchers exposed rat heart cells to 100-nanometer polystyrene nanoparticles and found that the particles were taken up by the cells and triggered a form of iron-dependent cell death called ferroptosis. The nanoparticles caused a buildup of reactive oxygen species in mitochondria, iron accumulation, and damage to cell membranes. The study suggests that nanoplastic exposure may pose risks to heart health through this specific cell death pathway.
Exposure to Polystyrene Nanoplastics Induces Ferroptosis-Associated Cardiac Injury: Cell-Based Evidence for Lysosome-Associated NLRX1 Loss and an NLRX1–STING–NCOA4 Response
AI summary Read the abstract
In mouse heart cells and in mice given polystyrene nanoplastics by mouth for eight weeks, the particles lowered the proteins NLRX1 and GPX4 and promoted iron buildup and lipid damage. The mice developed cardiac dysfunction and fibrosis.
HIF-1α/HO-1-Mediated Ferroptosis Participates in Polystyrene Nanoplastics-Induced Intergenerational Cardiotoxicity
AI summary Read the abstract
When pregnant mice were exposed to polystyrene nanoplastics, the particles crossed into offspring hearts and caused heart damage through a process called ferroptosis, a type of iron-dependent cell death. The nanoplastics activated a specific molecular pathway involving HIF-1 alpha and HO-1 that led to iron buildup, mitochondrial injury, and oxidative stress in heart tissue. This study raises concerns that maternal nanoplastic exposure during pregnancy could harm fetal heart development in ways that may have lasting consequences.
Inhaled polystyrene microplastics impaired lung function through pulmonary flora/TLR4-mediated iron homeostasis imbalance
AI summary Read the abstract
Mice that inhaled polystyrene microplastics for 60 days developed lung scarring, reduced lung function, and weakened lung barriers. The microplastics increased harmful bacteria in the lungs, which triggered an iron-related cell death process called ferroptosis -- revealing a new mechanism by which breathing in microplastics could cause lasting lung damage.
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.