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20 resultsShowing papers similar to Targeting GSTP1-dependent ferroptosis in lung cancer radiotherapy: Existing evidence and future directions
ClearThe interplay of ferroptosis and oxidative stress in pulmonary fibrosis: from mechanisms to treatment
This research review summarizes how a specific type of cell death called ferroptosis may contribute to pulmonary fibrosis, a serious lung disease where scar tissue builds up and makes breathing difficult. Scientists have found that when cells die from iron buildup and damage from harmful molecules, it can worsen lung scarring, but drugs that block this process show promise in animal studies. Understanding this connection could lead to new treatments for people with pulmonary fibrosis, though more research is needed to make sure these potential medicines are safe and effective in humans.
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.
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.
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.
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.
Polystyrene nanoplastics lead to ferroptosis in the lungs
Researchers found that polystyrene nanoplastics trigger ferroptosis — a type of iron-driven cell death — in the cells lining the lungs by activating a stress signaling pathway (HIF-1α/HO-1), ultimately causing lung tissue injury. This adds to growing evidence that inhaled nanoplastics can directly damage respiratory tissue through oxidative cell death mechanisms.
Double-edged Sword Role of Iron-loaded Ferritin in Extracellular Vesicles
This review explores the dual role of iron-loaded ferritin in extracellular vesicles, discussing how excess cellular iron promotes Fenton reaction-driven oxidative DNA damage and cellular ferroptosis resistance, contributing to carcinogenesis.
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.
Oridonin-induced ferroptosis and apoptosis: a dual approach to suppress the growth of osteosarcoma cell
This study investigated the anti-tumor effects of oridonin, a natural plant compound, on osteosarcoma cells, finding it triggered both ferroptosis and apoptosis to suppress tumor growth. While focused on cancer treatment rather than microplastics, the ferroptosis pathway studied is also implicated in cellular damage caused by microplastic exposure.
Inhalation exposure to cationic nanoplastic induces ferroptosis in the lung by perturbing core circadian transcription factors Bmal1
Researchers showed that inhaled cationic (positively charged, amino-modified) polystyrene nanoplastics trigger a form of iron-dependent cell death called ferroptosis in mouse lungs by suppressing the circadian clock protein Bmal1 and its downstream antioxidant pathway, and that a natural Bmal1 activator partially protected against the damage.
Polystyrene nanoplastics-induced lung epithelial cells ferroptosis promotes pulmonary fibrosis via YY1/FTL axis
Researchers found that polystyrene nanoplastics induced ferroptosis—an iron-dependent form of cell death—in lung bronchial epithelial cells and promoted pulmonary fibrosis in mice via the YY1/FTL signaling axis. The study identified ferroptosis as a novel mechanism underlying nanoplastic-induced lung injury and fibrosis, with potential therapeutic relevance for targeting this pathway.
Oridonin-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.
Targeting Regulated Cell Death Pathways in COPD: Mechanisms and Therapeutic Strategies
This review examines how multiple regulated cell death pathways — including apoptosis, necroptosis, pyroptosis, ferroptosis, and autophagy — contribute to chronic obstructive pulmonary disease progression and discusses these pathways as potential therapeutic targets.
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 nanoplastics-induced lung apoptosis and ferroptosis via ROS-dependent endoplasmic reticulum stress
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.
Polystyrene microplastics induce pulmonary fibrosis by promoting alveolar epithelial cell ferroptosis through cGAS/STING signaling
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.
Xenoferroptosis, a double-hit challenge for regulated cell death
This review explored xenoferroptosis—a form of regulated cell death driven by iron-dependent lipid peroxidation triggered by environmental contaminants including microplastics and heavy metals. The authors found that xenoferroptosis represents a double-hit mechanism linking environmental exposure to neurodegenerative diseases like Alzheimer's and Parkinson's.
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.