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61,005 resultsShowing papers similar to Oridonin-induced ferroptosis and apoptosis: a dual approach to suppress the growth of osteosarcoma cell
ClearOridonin-induced ferroptosis and apoptosis: a dual approach to suppress the growth of osteosarcoma cells
Researchers found that oridonin, a natural plant compound, can trigger two different types of cell death simultaneously in bone cancer cells. This dual mechanism makes it effective at suppressing tumor growth in osteosarcoma. The study suggests oridonin could be a promising therapeutic agent for treating this type of bone cancer.
Ferroptosis inhibition via the ROS-GPX4 axis drives microplastic-induced malignant progression of nasopharyngeal carcinoma
Researchers investigated how polystyrene microplastics promote malignant progression in nasopharyngeal carcinoma cells, finding that the plastics inhibit ferroptosis—an iron-dependent cell death pathway—via the ROS-GPX4 axis, thus allowing cancer cells to survive and proliferate. Blocking this anti-ferroptosis effect restored cancer cell death, suggesting that targeting the ferroptosis pathway could counteract microplastic-driven tumor progression.
Ferroptosis inhibition via the ROS-GPX4 axis drives microplastic-induced malignant progression of nasopharyngeal carcinoma
Researchers investigated how polystyrene microplastics promote malignant progression in nasopharyngeal carcinoma cells. The study found that microplastics inhibit ferroptosis (a form of regulated cell death) through the ROS-GPX4 signaling axis, enhancing cancer cell proliferation, migration, and invasion both in cell cultures and in animal models.
Ferroptosis inhibition via the ROS-GPX4 axis drives microplastic-induced malignant progression of nasopharyngeal carcinoma
Researchers investigated how polystyrene microplastics promote malignant progression in nasopharyngeal carcinoma cells. The study found that microplastics inhibit ferroptosis (a form of regulated cell death) through the ROS-GPX4 signaling axis, enhancing cancer cell proliferation, migration, and invasion both in cell cultures and in animal models.
Understanding the mechanistic roles of microplastics combined with heavy metals in regulating ferroptosis: Adding new paradigms regarding the links with diseases
This review explores the emerging connection between microplastics combined with heavy metals and a type of cell death called ferroptosis, which involves iron-dependent damage to cell membranes. Researchers found that both microplastics and heavy metals can independently trigger ferroptosis, and their combined presence may amplify this effect in organs like the liver, kidneys, and brain. The study suggests that understanding this cell death pathway could provide new insights into how environmental pollutant mixtures contribute to disease.
Polystyrene Microplastics Induce Radiotherapy Resistance in Lung Cancer by Suppressing Ferroptosis Through NF-κB Activation
Researchers found that polystyrene microplastics impaired radiotherapy efficacy in lung cancer cells by suppressing ferroptosis—a form of iron-dependent cell death—through NF-κB activation, providing the first evidence that microplastics may contribute to cancer therapy resistance.
Research progress on ferroptosis in the pathogenesis and treatment of neurodegenerative diseases
This review explores ferroptosis, a type of iron-dependent cell death that damages brain cells through fat oxidation, and its role in neurodegenerative diseases like Alzheimer's and Parkinson's. While not directly about microplastics, ferroptosis is one of the cellular damage pathways that microplastic exposure can trigger in brain tissue. Understanding how ferroptosis works may help explain how environmental pollutants, including nanoplastics that can cross the blood-brain barrier, contribute to neurological damage.
Ferroptosis induced by environmental pollutants and its health implications
Researchers reviewed how environmental pollutants — including microplastics, PM2.5, and heavy metals — trigger ferroptosis, a form of programmed cell death driven by iron and fat oxidation, finding that targeting this cell death pathway could be a strategy to reduce organ damage caused by pollution exposure.
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.
Research Progress on Micro(nano)plastic-Induced Programmed Cell Death Associated with Disease Risks
This review summarizes how micro and nanoplastics can trigger different types of programmed cell death, including ferroptosis, pyroptosis, and apoptosis, based on recent animal and cell studies. These forms of cell death are linked to inflammation and diseases affecting the gut, liver, lungs, brain, and reproductive system. The findings help explain the biological mechanisms through which microplastic exposure could contribute to chronic disease in humans.
Ferroptosis is the key cellular process mediating Bisphenol A responses in Chlamydomonas and a promising target for enhancing microalgae-based bioremediation
Researchers discovered that ferroptosis, a specific type of cell death involving iron and lipid damage, is the primary cellular mechanism through which bisphenol A (BPA) — a common microplastic component — harms green algae. By understanding this pathway, they identified potential targets for enhancing the ability of microalgae to break down BPA pollution. The findings could help improve algae-based bioremediation strategies for cleaning up plastic-related contaminants in water.
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.
Inhibiting ferroptosis in brain microvascular endothelial cells: A potential strategy to mitigate polystyrene nanoplastics‒induced blood‒brain barrier dysfunction
Researchers found that polystyrene nanoplastics disrupt the blood-brain barrier in mice by triggering ferroptosis — an iron-dependent form of cell death — in brain microvascular endothelial cells, and that blocking ferroptosis with a targeted drug reduced tight junction protein loss and restored barrier integrity.
International consensus guidelines for the definition, detection, and interpretation of autophagy-dependent ferroptosis
This scientific review provides guidelines for understanding a specific type of cell death called autophagy-dependent ferroptosis, where cells essentially digest their own protective components and then die from iron-driven damage. While not directly about microplastics, this process is relevant because microplastics and nanoplastics have been shown to trigger oxidative stress and iron-related cell damage in tissues. Understanding these cell death pathways helps researchers assess how plastic particle exposure could harm organs like the liver, brain, and lungs.
Cancer Metabolism: The Role of ROS in DNA Damage and Induction of Apoptosis in Cancer Cells
This review explores how reactive oxygen species (ROS) -- harmful molecules produced during abnormal cell metabolism -- can damage DNA and trigger cancer cell death, making ROS a potential target for cancer treatment. While not directly about microplastics, this is relevant because microplastic exposure is known to increase ROS production in human cells, which could contribute to DNA damage over time.
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.
Polystyrene nanoplastics disrupt iron homeostasis by promoting FPN1 ubiquitination in GC-2spd(ts) cells
Researchers showed that polystyrene nanoplastics induce ferroptosis — an iron-dependent form of cell death — in mouse sperm precursor cells by promoting the ubiquitin-tagged degradation of the iron-export protein ferroportin1, causing iron to accumulate inside cells, driving lipid peroxidation and mitochondrial damage.
Unravelling the Potential Role of Nanoplastics and Microplastics‐Induced Toxicity in Freshwater Fish: Emerging Role of Programmed Cell Death Mechanisms
This review examines how micro- and nanoplastics trigger various forms of programmed cell death in freshwater fish, including apoptosis, autophagy, ferroptosis, and pyroptosis. The study highlights that exposure to these plastic particles generates oxidative stress, inflammation, and DNA damage, with the resulting cell death mechanisms potentially compromising fish health and raising concerns about contamination reaching humans through seafood consumption.
Ferroptosis and Wnt/β-Catenin Signaling Triggered by Environmentally Relevant Nanoscale Polypropylene Plastics in Human Intestinal Models
Researchers exposed human intestinal organoids and epithelial cells to environmentally weathered nanoscale polypropylene particles, finding they induce ferroptosis as the primary cell death pathway alongside Wnt/beta-catenin activation as a compensatory protective response, highlighting the importance of using realistic aged nanoplastics and 3D organoid models in health risk assessments.
BRCC36 Deubiquitinates HMGCR to Regulate the Interplay Between Ferroptosis and Pyroptosis
This study uncovered a molecular switch (an enzyme called BRCC36) that controls whether liver cancer cells die by ferroptosis or pyroptosis, two different forms of programmed cell death. While not directly about microplastics, ferroptosis has been identified as one of the ways nanoplastics damage cells in recent studies. Understanding how cells regulate ferroptosis could help explain why some tissues are more vulnerable to nanoplastic-induced damage than others.
Additional file 3 of Ferroptosis inhibition via the ROS-GPX4 axis drives microplastic-induced malignant progression of nasopharyngeal carcinoma
This is a supplementary material file (Additional File 3) attached to a study on microplastics and cancer progression — not an independent paper with findings to summarize.
Additional file 3 of Ferroptosis inhibition via the ROS-GPX4 axis drives microplastic-induced malignant progression of nasopharyngeal carcinoma
This is a supplementary material file (Additional File 3) attached to a study on microplastics and cancer progression — not an independent paper with findings to summarize.
Molecular mechanism differences between nanoplastics and microplastics in colon toxicity: nanoplastics induce ferroptosis-mediated immunogenic cell death, while microplastics cause cell metabolic reprogramming
This study discovered that nanoplastics and microplastics damage the colon through completely different mechanisms depending on their size: nanoscale particles (100 nm) get inside cells and trigger a type of cell death called ferroptosis, while larger particles (10 micrometers) cause physical damage and force cells to switch their energy production. These findings suggest that the smallest plastic particles may pose unique health risks to the gut that differ from larger ones.
Additional file 2 of Ferroptosis inhibition via the ROS-GPX4 axis drives microplastic-induced malignant progression of nasopharyngeal carcinoma
This is a supplementary material file (Additional File 2) attached to a study on microplastics and cancer progression — not an independent paper with findings to summarize.