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61,005 resultsShowing papers similar to Iron's silent betrayal: Ferritinophagy-driven mitochondrial damage mediates polylactic acid nanoplastics and Cr(VI)-induced cardiac injury
ClearSynergistic kidney toxicity of polylactic acid nanoplastics and Cr(VI): Ferroptosis aggravated by mitophagy
Researchers investigated the combined kidney toxicity of polylactic acid nanoplastics and hexavalent chromium in mice. The study found that co-exposure produced synergistic kidney damage through ferroptosis aggravated by mitophagy, suggesting that even bioplastic-derived nanoplastics can enhance heavy metal toxicity when both contaminants are present together.
The “Butterfly Effect” of heart failure: Induced by the combination of polylactic acid nanoplastics and copper from the perspective of gut microbiome
Researchers investigated how co-exposure to polylactic acid nanoplastics and copper disrupts the gut-heart axis in mice, finding that combined exposure caused greater heart failure severity than either substance alone. Gut microbiota dysbiosis emerged as a mediating pathway linking intestinal exposure to cardiac dysfunction.
The mediating role of ferroptosis and mitochondrial dynamics disorder in the aggravation of cardiac injury by polystyrene microplastics
Researchers investigated how polystyrene microplastics worsen heart injury in mice, particularly when combined with the chemotherapy drug doxorubicin. The study found that microplastics aggravated cardiac damage through ferroptosis and mitochondrial dysfunction pathways, and that two protective compounds, Ferrostatin-1 and luteolin, showed potential in mitigating these harmful effects on heart tissue.
Novel insights into male reproductive toxicity: autophagy-dependent ferroptosis triggered by polylactic acid nanoplastics and copper sulfate
Researchers exposed mice to polylactic acid nanoplastics combined with copper sulfate and found that the combination caused significant testicular damage through a process linking autophagy to ferroptosis, a form of iron-dependent cell death. The combined exposure was more damaging than either substance alone, disrupting sperm production and testicular tissue structure. The study suggests that nanoplastics from biodegradable plastics may amplify the reproductive toxicity of environmental heavy metals.
Ferroptosis and hepatic fibrosis induced by cooperative exposure to polylactic acid nanoplastics and copper: Emphasis on gut microbiota dysbiosis
Researchers investigated the combined hepatotoxicity of polylactic acid nanoplastics and copper in mice, focusing on the gut-liver axis. The study found that co-exposure caused synergistic liver damage through ferroptosis, characterized by disrupted glutathione and iron homeostasis, along with gut microbiota dysbiosis and hepatic fibrosis more severe than either pollutant alone.
Exposure of polystyrene nanoplastics led to ferroptosis on cardiomyocytes
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.
Ferroptosis involved in inhaled polystyrene microplastics leaded myocardial fibrosis through HIF-ROS-SLC7A11/GPX4 Pathway
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.
Realistic Nanoplastics Induced Pulmonary Damage via the Crosstalk of Ferritinophagy and Mitochondrial Dysfunction
Researchers created realistic nanoplastics by mechanically breaking down bulk plastic rather than using lab-made particles, and found that inhaling these particles caused significant lung damage in mice through iron-related cell death and mitochondrial dysfunction. PVC nanoplastics were the most harmful of the four types tested, and all were more toxic than commonly used lab-standard polystyrene spheres, suggesting previous studies may have underestimated the lung health risks of airborne nanoplastics.
HIF-1α/HO-1-Mediated Ferroptosis Participates in Polystyrene Nanoplastics-Induced Intergenerational Cardiotoxicity
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.
Adolescent exposure to polylactic acid microplastics causes cardiac fibrosis by promoting cardiomyocyte senescence
Adolescent mice exposed to polylactic acid (PLA) biodegradable microplastics developed cardiac fibrosis, with mechanistic studies showing that PLA particles promoted cardiomyocyte senescence and activated inflammatory signaling, demonstrating cardiotoxicity from a supposedly 'green' plastic.
Co-exposure of arsenic and polystyrene-nanoplastics induced kidney injury by disrupting mitochondrial homeostasis and mtROS-mediated ferritinophagy and ferroptosis
Researchers found that arsenic and polystyrene nanoplastics together — but not separately — cause kidney fibrosis in mice by disrupting mitochondrial function and triggering a form of iron-dependent cell death called ferroptosis, with mitochondria-targeted antioxidants significantly reducing the combined damage.
Polystyrene nanoplastics and cadmium co-exposure aggravated cardiomyocyte damage in mice by regulating PANoptosis pathway
Researchers gave mice low doses of polystyrene nanoplastics and cadmium (a toxic metal) together and found that the combination caused significantly worse heart damage than either substance alone. The damage involved a newly recognized form of cell death called PANoptosis, which combines multiple destructive pathways in heart cells. This suggests that real-world exposure to nanoplastics alongside common environmental pollutants like cadmium could compound risks to heart health.
Polystyrene nanoplastics exacerbate lipopolysaccharide-induced myocardial fibrosis and autophagy in mice via ROS/TGF-β1/Smad
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.
Realistic-NPs trigger depression-like behaviors via mitochondrial iron overload mediating ferroptosis
Researchers created environmentally realistic nanoplastics by mechanically fragmenting polystyrene and found that exposing mice to these particles induced depression-like behaviors within two weeks, along with later learning and memory deficits. The study identified mitochondrial iron overload and ferroptosis in the brain as the underlying mechanism, with the iron chelator deferoxamine able to reverse these effects.
Polystyrene nanoplastics trigger mitochondrial and metabolic reprogramming in cardiomyocytes: Evidence from integrated transcriptomic and metabolomic analysis
Scientists found that tiny plastic particles called nanoplastics can damage heart cells by disrupting their powerhouses (mitochondria) and reducing their ability to produce energy. When researchers exposed human heart cells and mice to these nanoplastics, they observed weakened heart function and signs of early heart damage. This research suggests that the growing amount of microscopic plastic pollution in our environment could pose previously unknown risks to heart health.
Ferritinophagy Mediated by Oxidative Stress-Driven Mitochondrial Damage Is Involved in the Polystyrene Nanoparticles-Induced Ferroptosis of Lung Injury
Researchers found that inhaled polystyrene nanoplastics cause lung damage through a specific cell death process called ferroptosis, which involves iron buildup and oxidative stress in lung cells. The nanoplastics damaged mitochondria and triggered a chain reaction where the cell's iron storage was broken down, releasing harmful iron. Blocking this ferroptosis process with a drug called ferrostatin-1 reversed the lung damage in mice, pointing to a potential treatment approach.
Microplastics and nanoplastics co-exposure modulates chromium bioaccumulation and physiological responses in rats
Rats exposed to a mix of microplastics and nanoplastics along with hexavalent chromium, a toxic heavy metal, accumulated significantly more chromium in their liver, heart, brain, and skin than rats exposed to chromium alone. This shows that plastic particles can act as carriers that increase the amount of toxic metals absorbed by the body, potentially amplifying the health risks of metal pollution.
Sight of Aged Microplastics Adsorbing Heavy Metal Exacerbated Intestinal Injury: A Mechanistic Study of Autophagy-Mediated Toxicity Response
When mice were exposed to aged microplastics carrying chromium (a toxic heavy metal), they experienced severe intestinal damage, inflammation, and increased vulnerability to bacterial infections. The microplastics intensified the harm because stomach acid released the chromium from the plastic surface, triggering a dangerous cycle of oxidative stress and cell death in the gut lining.
Co-exposure to environmentally relevant concentrations of cadmium and polystyrene nanoplastics induced oxidative stress, ferroptosis and excessive mitophagy in mice kidney
A mouse study found that combined exposure to cadmium (a toxic metal) and polystyrene nanoplastics caused more kidney damage than either pollutant alone. The combination triggered a harmful chain reaction involving oxidative stress, iron buildup, and excessive breakdown of cellular energy factories called mitochondria. This is significant because people are often exposed to both nanoplastics and heavy metals simultaneously, and their combined effects may be worse than expected.
Microplastics induce mitochondrial dysfunction and accelerate cardiovascular pathogenesis
Researchers reviewed evidence that micro- and nanoplastics detected in human cardiovascular tissues may contribute to cardiovascular disease through mitochondrial dysfunction. The study found that these particles can impair mitochondrial integrity, induce oxidative stress, disrupt calcium signaling, and promote genomic instability, suggesting a mechanistic link between plastic particle exposure and cardiovascular pathology.
Co-exposure of polystyrene microplastics and iron aggravates cognitive decline in aging mice via ferroptosis induction
Researchers studied the combined effects of microplastic and iron exposure on cognitive function in aging mice. They found that polystyrene microplastics accumulated in the brain's cortex and hippocampus, and when combined with iron, significantly worsened cognitive decline through a cell death process called ferroptosis. The study suggests that co-exposure to microplastics and metals may pose heightened risks to brain health in aging populations.
Synergistic effects of PS-NPs and Cd on ovarian toxicity in adolescent rats: Ferroptosis by induction of mitochondrial redox imbalance via the SIRT3-SOD2/Gpx4 pathway
Researchers studied the combined effects of polystyrene nanoplastics and cadmium on the ovaries of adolescent rats over 28 days. They found that co-exposure was significantly more harmful than either pollutant alone, causing damage to ovarian structure and hormone disruption through a process called ferroptosis triggered by mitochondrial oxidative stress. The study suggests that nanoplastics may act as a carrier that amplifies heavy metal toxicity to the reproductive system during critical developmental periods.
Polystyrene exacerbates cadmium‐induced mitochondrial damage to lung by blocking autophagy in mice
Researchers found that polystyrene microplastics exacerbated cadmium-induced mitochondrial damage in mouse lungs by blocking autophagy, revealing a synergistic toxicity mechanism when these two common environmental contaminants co-occur.
Microplastics induced inflammation and apoptosis via ferroptosis and the NF-κB pathway in carp
Researchers exposed carp to polyethylene microplastics and found they caused serious intestinal damage through two harmful pathways: ferroptosis (a type of iron-dependent cell death) and NF-kB-driven inflammation. The microplastics triggered a buildup of iron and reactive oxygen species in gut tissue, leading to cell death and tissue destruction. Since humans also ingest microplastics that reach the gut, these findings highlight a potential mechanism by which microplastics could damage our digestive system.