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61,005 resultsShowing papers similar to Targeting Regulated Cell Death Pathways in COPD: Mechanisms and Therapeutic Strategies
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.
Advances in the regulatory mechanisms of mTOR in necroptosis
This review explores how the mTOR signaling pathway regulates necroptosis, a form of programmed cell death distinct from apoptosis. Researchers describe multiple mechanisms through which mTOR influences cell death, including direct regulation of key necroptosis proteins, indirect effects through autophagy, and modulation of reactive oxygen species. The study highlights that mTOR can both promote and inhibit necroptosis depending on the context, making it a complex but promising therapeutic target.
Mitochondrial dysfunction–induced PANoptosis: Mechanisms, triggers, and disease implications
This review provides a comprehensive overview of PANoptosis, a recently identified form of cell death that combines features of three previously distinct pathways: pyroptosis, apoptosis, and necroptosis. Researchers describe how mitochondrial dysfunction can trigger this integrated cell death response, with implications for infections, inflammation, cancer, and degenerative diseases. The study highlights PANoptosis as an important emerging concept for understanding how cells respond to environmental and biological stressors.
Microplastics exacerbate ferroptosis via mitochondrial reactive oxygen species-mediated autophagy in chronic obstructive pulmonary disease
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.
Bibliometric analysis of global research trends on pyroptosis in lung disease
This bibliometric analysis mapped global research trends on pyroptosis (inflammatory cell death) in lung disease from 2000 to the present, identifying key countries, institutions, and collaboration networks driving this emerging field. The analysis shows growing research attention on the link between pyroptosis and acute lung injury, with future focus likely to expand to other lung conditions.
A bibliometric analysis of autophagy in lung diseases from 2012 to 2021
This bibliometric analysis maps autophagy research in lung diseases from 2012 to 2021, identifying key research hotspots, collaboration networks, and emerging trends linking autophagy mechanisms to various pulmonary conditions.
A Comprehensive Review on Cell Death
This paper is not about microplastics. It is a comprehensive review of different types of cell death including apoptosis, necrosis, necroptosis, autophagy, and cornification, explaining their mechanisms and biological roles. The study is focused on cell biology and pathophysiology with no connection to microplastic pollution or environmental health.
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.
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.
Mitochondrial Dysfunction and Nanocarrier-Based Treatments in Chronic Obstructive Pulmonary Disease (COPD)
This review examines how mitochondrial dysfunction contributes to the development and progression of chronic obstructive pulmonary disease. Researchers highlight emerging nanocarrier-based drug delivery systems designed to target mitochondrial dysfunction in lung tissue. The study suggests these novel nanoparticle approaches, while still in early clinical stages, represent a promising direction for future treatments.
Nanomaterial-induced pyroptosis: a cell type-specific perspective
This review examined how various nanomaterials induce pyroptosis (inflammatory cell death) across different non-tumorous cell types, analyzing the diverse pathways and mechanisms involved. The review highlights significant knowledge gaps regarding less-studied pyroptosis pathways and calls for more systematic investigation of nanomaterial-cell interactions.
Pollutant-induced pyroptosis in humans and other animals
This review examines how environmental pollutants including particulate matter, cadmium, and polystyrene microplastics trigger pyroptosis, a pro-inflammatory form of cell death, across diverse tissues in mammals and birds.
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.
The role of pyroptosis in inflammatory diseases
This review explains pyroptosis, a type of programmed cell death that triggers strong inflammation, and its role in diseases like infections, autoimmune conditions, and organ damage. While not focused on microplastics specifically, pyroptosis is one of the key mechanisms through which microplastic exposure may cause inflammation in tissues. Understanding this process helps explain how tiny plastic particles could trigger harmful immune responses in the body.
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.
Targeting GSTP1-dependent ferroptosis in lung cancer radiotherapy: Existing evidence and future directions
This review explores the relationship between the protein GSTP1, ferroptosis (a form of iron-dependent cell death), and radiotherapy resistance in lung cancer. Researchers propose that targeting GSTP1 could help overcome tumor cell resistance to radiation by promoting ferroptosis. While focused on cancer treatment mechanisms, the study touches on how environmental factors and oxidative stress pathways relevant to pollutant exposure intersect with cellular defense mechanisms.
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.
Beyond apoptosis: evidence of other regulated cell death pathways in the ovary throughout development and life
This review explores different types of programmed cell death in the ovary beyond the well-known process of apoptosis, and their roles in ovarian development and function throughout a woman's life. While not focused on microplastics directly, these cell death pathways are important because emerging research shows that microplastic and nanoplastic exposure can trigger abnormal cell death in ovarian tissue. Understanding these pathways is key to assessing how environmental pollutants may affect female fertility.
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.
Epigenetic regulation of pulmonary inflammation
Researchers reviewed how environmental exposures drive epigenetic changes — including DNA methylation, histone modifications, and non-coding RNA transfers via extracellular vesicles — that promote chronic lung diseases such as COPD, asthma, and pulmonary fibrosis, while also identifying these same epigenetic pathways as promising therapeutic targets.
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.
Dasatinib suppresses particulate-induced pyroptosis and acute lung inflammation
Researchers found that dasatinib, a tyrosine kinase inhibitor, suppressed NLRP3 inflammasome activation and pyroptosis (inflammatory cell death) induced by various industrial and environmental particulates including silica, asbestos, and carbon nanotubes in macrophages. The results identify a potential pharmacological approach to treating particulate matter-induced inflammatory lung diseases.
Gasdermin D-dependent macrophage pyroptosis mediates polystyrene microplastics-induced pulmonary fibrosis
Researchers demonstrated that chronic intranasal exposure to polystyrene microplastics in mice triggered a specific form of inflammatory cell death called pyroptosis in lung macrophages, leading to pulmonary fibrosis. The study identified the Gasdermin D protein as a key mediator of this process, suggesting a potential mechanistic pathway through which microplastic inhalation could contribute to lung tissue scarring.
Mechanism of Pyroptosis in Acute Liver Injury and Prospect of Targeted Therapy
This review examined the role of pyroptosis—an inflammatory form of programmed cell death—in acute liver injury, covering the gasdermin-mediated molecular mechanisms involved. The authors proposed that targeting pyroptosis pathways may offer new therapeutic strategies for conditions such as drug-induced liver injury and ischemia-reperfusion damage.