We can't find the internet
Attempting to reconnect
Something went wrong!
Hang in there while we get back on track
Mechanism of S-Palmitoylation in Polystyrene Nanoplastics-Induced Macrophage Cuproptosis Contributing to Emphysema through Alveolar Epithelial Cell Pyroptosis
AI summary Read the abstract
Researchers found that breathing in polystyrene nanoplastics caused emphysema (a type of lung disease) in rats by triggering a chain reaction: the nanoplastics entered immune cells in the lungs, caused copper-related cell death in those immune cells, which then released inflammatory signals that destroyed the air sacs. This newly discovered mechanism shows how inhaled nanoplastics could contribute to serious, irreversible lung damage.
More than microplastics, nanoplastics may pose a greater toxic effect on humans due to their unique physicochemical properties. Currently, research on lung diseases caused by respiratory exposure to nanoplastics is scarce, with epigenetic mechanisms warranting further investigation. In the present study, we exposed rats to polystyrene nanoplastics (PS-NPs) via an oral-nasal exposure system and found that PS-NPs exposure resulted in emphysema. Mechanistically, PS-NPs entered macrophages and competitively bound to sigma nonopioid intracellular receptor 1 (SIGMAR1), leading to an increase in free zDHHC palmitoyltransferase 14 (zDHHC14). This, in turn, caused elevated palmitoylation of solute carrier family 31 member 1 (SLC31A1) in macrophages, inhibiting its ubiquitination and degradation, thereby enhancing SLC31A1 expression. The increased expression of SLC31A1 promoted cuproptosis of macrophages and elevated tumor necrosis factor-α (TNF-α) secretion, which activated the NLR family pyrin domain containing 3/matrix metallopeptidase 9 (NLRP3/MMP-9) pathway in alveolar epithelial cells (AECs). This process mediated pyroptosis and degradation of extracellular matrix (ECM), resulting in the destruction of alveolar structure and development of emphysema. The findings demonstrate a previously unknown molecular mechanism by which PS-NPs induce emphysema. The findings have implications for the prevention and treatment of respiratory system damage caused by nanoparticles.
More Papers Like This
Mechanismof S‑Palmitoylationin Polystyrene Nanoplastics-Induced Macrophage Cuproptosis Contributingto Emphysema through Alveolar Epithelial Cell Pyroptosis
AI summary Read the abstract
Researchers identified S-palmitoylation—a lipid modification process—as a key mechanism by which inhaled polystyrene nanoplastics trigger macrophage ferroptosis (iron-dependent cell death) in the lungs, providing a molecular explanation for how respiratory nanoplastic exposure damages immune cells.
Inhalation exposure to polystyrene nanoplastics induces chronic obstructive pulmonary disease-like lung injury in mice through multi-dimensional assessment
AI summary Read the abstract
Mice that inhaled polystyrene nanoplastics developed lung damage resembling chronic obstructive pulmonary disease (COPD), including reduced breathing function, inflammation, and oxidative stress that worsened with longer exposure. The study found that nanoplastics caused this damage by disrupting mitochondria and triggering a type of cell death called ferroptosis, suggesting that breathing in airborne nanoplastics could increase the risk of serious lung disease.
Polystyrene nanoplastics-induced lung apoptosis and ferroptosis via ROS-dependent endoplasmic reticulum stress
AI summary Read the abstract
This study found that polystyrene nanoplastics cause lung cell death through two pathways: apoptosis (programmed cell death) and ferroptosis (iron-dependent cell death), both triggered by oxidative stress in the cell's endoplasmic reticulum. The damage was observed both in human lung cells in the lab and in mice exposed to the nanoplastics. Importantly, the antioxidant NAC (N-acetylcysteine) reduced both types of cell death, suggesting it could help protect lungs from nanoplastic damage.
Microplastics exacerbate ferroptosis via mitochondrial reactive oxygen species-mediated autophagy in chronic obstructive pulmonary disease
AI summary Read the abstract
Researchers found that microplastics worsen chronic obstructive pulmonary disease (COPD) by triggering a chain reaction in lung cells: the plastics damage mitochondria (the cell's energy centers), which produces harmful molecules that activate a self-destructive process called autophagy-dependent ferroptosis. Lung tissue from COPD patients contained significantly higher concentrations of polystyrene microplastics than healthy controls. When scientists blocked this destructive pathway in mice, it reduced the excessive inflammation and prevented COPD flare-ups caused by microplastic exposure.
Polystyrene nanoplastics induce pulmonary oxidative stress and programmed cell death through the cGAS-STING-NLRP3 pathway
AI summary Read the abstract
Researchers exposed mice to polystyrene nanoplastics through nasal administration and studied the resulting lung damage over seven days. They found that the nanoplastics triggered oxidative stress, programmed cell death, and inflammatory responses in lung tissue through activation of the cGAS-STING-NLRP3 signaling pathway. The study provides evidence that inhaled nanoplastics can cause acute lung injury through specific molecular mechanisms involving both apoptosis and pyroptosis.
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.