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Pollutant-induced pyroptosis in humans and other animals
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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.
Pyroptosis is a form of lytic cell death with pro-inflammatory characteristics, induced upon the activation of certain inflammatory caspases by inflammasome complexes such as NLRP3 inflammasome. Gasdermin proteins as the mediators of pyroptosis form cell membrane pores upon activation, which release certain cellular contents into the extracellular space including inflammatory cytokines such as IL-1β and IL-18, and also damage the integrity of the cell membrane. Gasdermins have been implicated in autoimmune and inflammatory diseases, infectious diseases, deafness and cancer. Mostly in the last 2 years, diverse pollutant types including particulate matter, cadmium and polystyrene microplastics were reported to induce pyroptotic cell death in diverse tissues from mammals to birds. In the present study, we review our current understanding of pollutant-induced pyroptosis as well as current knowledge of upstream events leading to pyroptotic cell death upon exposure to pollutants.
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Exposure to Polystyrene Microplastics Promotes the Progression of Cognitive Impairment in Alzheimer’s Disease: Association with Induction of Microglial Pyroptosis
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In a mouse study, polystyrene microplastics worsened cognitive decline in an Alzheimer's disease model by triggering a type of inflammatory cell death called pyroptosis in brain immune cells. The microplastics caused brain inflammation that accelerated memory loss and cognitive impairment beyond what Alzheimer's alone caused. This is one of the first studies suggesting that microplastic exposure could make neurodegenerative diseases like Alzheimer's progress faster.
Understanding the mechanistic roles of microplastics combined with heavy metals in regulating ferroptosis: Adding new paradigms regarding the links with diseases
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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 exposure aggravates acute liver injury by promoting Kupffer cell pyroptosis
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Researchers found that long-term exposure to polystyrene microplastics worsened acute liver injury in mice by triggering a specific type of inflammatory cell death called pyroptosis in liver immune cells. When they blocked this cell death pathway either genetically or with a drug, the damaging effects of the microplastics were significantly reduced. The study suggests that microplastic exposure may make the liver more vulnerable to injury by amplifying inflammatory responses.
Co-exposure of cadmium and polystyrene nanoplastics: Induction pyroptosis and autophagy in mice testis
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Researchers investigated the combined effects of cadmium and polystyrene nanoplastics on mouse testicular tissue. The study found that co-exposure produced more severe testicular damage than either substance alone, driven by the interplay between pyroptosis (inflammatory cell death) and autophagy. Inhibiting one of these cellular processes affected the other, suggesting they are closely interconnected in the toxicity response to nanoplastic and heavy metal co-exposure.
Recent consequences of micro-nanaoplastics (MNPLs) in subcellular/molecular environmental pollution toxicity on human and animals
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This review examines the subcellular and molecular mechanisms by which micro- and nanoplastics cause toxicity in humans and animals, focusing on oxidative stress, inflammation, cell death pathways, and endocrine disruption at the cellular level.
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When a large batch of papers lands in the Atlas, we read through it and send a short write-up of what stood out.