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61,005 resultsShowing papers similar to Transcriptome-wide m6A modification mediates cardiotoxicity in mice after chronic exposure to microplastics
ClearN6-methyladenosine methylation mediates non-coding RNAs modification in microplastic-induced cardiac injury
Researchers found that microplastic exposure in mice led to accumulation in organs and triggered cell death, particularly affecting heart tissue. Using advanced sequencing techniques, they discovered that microplastics altered chemical modifications (m6A methylation) on non-coding RNA molecules in heart cells, which may disrupt important gene regulatory networks. The study suggests a potential molecular mechanism through which microplastic exposure could contribute to heart damage, though more research is needed to understand the full implications.
Microplastic exposure is associated with epigenomic effects in the model organism Pimephales promelas (fathead minnow)
Researchers exposed fathead minnows to microplastics and found changes in DNA methylation -- a chemical modification that controls which genes are turned on or off -- across multiple organs including the brain, liver, and gonads. These epigenetic changes are heritable, meaning microplastic exposure could affect not just the exposed fish but also future generations, raising concerns about long-term ecological and evolutionary impacts.
Beyond genetics: can micro and nanoplastics induce epigenetic and gene-expression modifications?
This review gathers existing research on whether micro and nanoplastics can cause epigenetic changes, which are modifications that alter how genes work without changing the DNA itself. Although studies are still limited, the evidence so far shows that both short-term and long-term plastic particle exposure can trigger these gene-level changes in various organisms. This is concerning because epigenetic changes can potentially be passed to future generations and may contribute to disease.
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.
Changes in global methylation patterns of Mytilus galloprovincialis exposed to microplastics
Researchers found that exposing mussels to polystyrene microplastics caused changes in their DNA methylation patterns, an epigenetic modification that controls how genes are turned on and off. Higher microplastic concentrations led to greater loss of methylation, and similar patterns were seen in wild mussels from polluted areas. This suggests microplastics could affect organisms at the genetic regulation level, potentially influencing metabolism and cell division.
Nanoplastics as Epigenetic Disruptors: A Biochemical Review of Environmental Pollutants and Gene Regulation
This biochemical review examined how nanoplastics disrupt epigenetic regulation, focusing on their ability to alter DNA methylation patterns, histone modifications, and non-coding RNA expression. The authors argued that nanoplastic-induced epigenetic changes could have lasting developmental and health consequences, especially during vulnerable life stages.
Environmental Xenobiotics and Epigenetic Modifications: Implications for Human Health and Disease
This review examines how environmental pollutants, including microplastics, can change gene activity through epigenetic modifications without altering DNA itself. These changes to how genes are turned on and off can contribute to cancer, brain diseases, and developmental problems, and may even be passed down to future generations. The research highlights that microplastics and other common pollutants could have long-lasting health effects that go beyond direct chemical toxicity.
Epigenetic and Gene Expression Responses in Daphnia magna to Polyethylene and Polystyrene Microplastics
Researchers exposed water fleas (Daphnia magna) to polyethylene and polystyrene microplastics and examined changes at the genetic and molecular level. They found that the microplastics altered DNA methylation patterns and disrupted the expression of genes involved in reproduction and stress response. The study provides evidence that microplastic exposure can cause changes beyond physical harm, affecting organisms at the epigenetic level.
Molecular Landscape Remodeling Unravels the Cross-Links of Microplastics-Induced Lipidomic Fluctuations, Nutrient Disorders and Energy Disarrangements
Researchers fed mice polypropylene microplastics chronically and used lipidomics and transcriptomics to show that microplastics accumulated in the liver and disrupted lipid metabolism, cholesterol homeostasis, and redox balance, with high doses causing fibrotic liver changes.
Emerging cardiovascular risks of micro- and nanoplastics: toxic effects and mechanistic pathways
Tiny plastic particles called micro- and nanoplastics are getting into our bodies through food, air, and skin contact, and researchers have found them building up in people's hearts and blood vessels. This review of existing studies shows these plastic bits may contribute to heart disease by causing inflammation and damaging cells in the cardiovascular system. While more research is needed, this suggests that plastic pollution isn't just an environmental problem—it could be directly harming our heart health.
Molecular LandscapeRemodeling Unravels the Cross-Linksof Microplastics-Induced Lipidomic Fluctuations,Nutrient Disorders and Energy Disarrangements
This study assessed the liver toxicity of polypropylene microplastics in mice using combined lipidomics and transcriptomics, identifying disrupted lipid metabolism, altered cholesterol handling, and fibrotic tissue remodeling as key pathological outcomes.
Investigating the Epigenetic Effects of Polystyrene Nanoplastic Exposure in Bluegill (Lepomis macrochirus) Epithelial Cells Using Methylation-Sensitive AFLPs
Researchers exposed bluegill fish cells to polystyrene nanoplastics and examined whether the exposure caused changes in DNA methylation, a type of genetic modification that can alter how genes function. They found that nanoplastic exposure did cause methylation changes across the genome, but the effect was not dependent on dose or exposure time -- simply being exposed to nanoplastics was enough to trigger the changes. The findings suggest that even low-level nanoplastic exposure could have epigenetic effects on aquatic organisms.
Micro(nano)plastics in the brain: Epigenetic perturbations in progression to neurodegenerative diseases.
This review examined how micro(nano)plastics (MNPs) accumulate in the brain and induce epigenetic changes—including DNA methylation and histone modification—that may drive the progression of neurodegenerative diseases. MNPs were found to disrupt neuronal homeostasis through multiple epigenetic mechanisms after crossing the blood-brain barrier.
Molecular LandscapeRemodeling Unravels the Cross-Linksof Microplastics-Induced Lipidomic Fluctuations,Nutrient Disorders and Energy Disarrangements
Researchers examined polypropylene microplastic retention in mouse liver using lipidomics and transcriptomics, finding that chronic exposure disrupted lipid metabolism, cholesterol turnover, and antioxidant defense, with high-dose treatment causing regional liver fibrosis.
Epigenetics of Microplastics
This student-authored paper reviews how microplastics and nanoplastics (MNPs) can alter gene expression and enzyme activity in animals, with particular concern for effects on the liver, brain, and male reproductive system. MNPs act as carriers for toxic chemicals like BPA, phthalates, and heavy metals, which can trigger inflammation, oxidative stress, and potentially cancer when ingested by humans. The paper highlights that human exposure is already occurring through contaminated soil, water, and food, making understanding these epigenetic risks an urgent public health priority.
Mechanism of Nano‐Microplastics Exposure‐Induced Myocardial Fibrosis: DKK3‐Mediated Mitophagy Dysfunction and Pyroptosis
Researchers investigated how nano-microplastic exposure leads to heart tissue scarring in mice and identified a specific molecular pathway involved. They found that the plastic particles suppressed a protein called DKK3, which disrupted the cell's ability to recycle damaged mitochondria, triggering an inflammatory cell death process that promotes fibrosis. The study reveals a potential mechanism by which long-term microplastic exposure could contribute to cardiac damage.
A systematic review on the impact of micro-nanoplastics on human health: Potential modulation of epigenetic mechanisms and identification of biomarkers
This systematic review found that micro-nanoplastic exposure can trigger epigenetic modifications including chromatin remodeling and miRNA modulation, with potential effects on the KSR-ERK-MAPK, FOXO-Insulin, and GPX3-HIF-alpha pathways in humans. These epigenetic changes could disrupt glucose balance, apoptosis, cell proliferation, and immune function, and may be heritable through mitosis, raising concerns about transgenerational health effects.
Systematic Review: Efek Nanoplastik terhadap Metilasi DNA pada Manusia
This systematic review, written in Indonesian, examines how nanoplastics may affect DNA methylation in humans — a process that controls which genes are turned on or off. Changes in DNA methylation can influence disease risk, including cancer. The review highlights an important but understudied pathway through which tiny plastic particles could affect human health at the genetic level.
Epigenetic mechanisms of particulate matter exposure: air pollution and hazards on human health
This review examines how breathing in particulate matter from air pollution -- which can include microplastic particles -- causes lasting health damage through epigenetic changes, meaning it alters how genes are turned on and off without changing the DNA itself. These changes have been linked to cancer, lung scarring, brain diseases, and metabolic disorders. The findings suggest that airborne microplastics could contribute to disease through similar epigenetic mechanisms.
Molecular LandscapeRemodeling Unravels the Cross-Linksof Microplastics-Induced Lipidomic Fluctuations,Nutrient Disorders and Energy Disarrangements
Researchers used combined lipidomic and transcriptomic analysis to demonstrate that polypropylene microplastics accumulated in mouse liver and disrupted key metabolic pathways including lipid biosynthesis, cholesterol metabolism, and energy homeostasis.
The cardiovascular toxicity of polystyrene microplastics in rats: based on untargeted metabolomics analysis
A rat study using metabolomics analysis found that long-term exposure to high concentrations of polystyrene microplastics led to abnormal fat metabolism and cardiovascular damage. The harm appeared to be driven by oxidative stress and inflammation, suggesting that chronic microplastic exposure could contribute to heart and blood vessel disease.
Tiny trouble: microplastics, nanoplastics, and their heartfelt impact on cardiovascular health
This review summarizes growing evidence that microplastics and nanoplastics have been found in human heart tissue, arterial plaques, and blood, and may increase the risk of cardiovascular disease. Lab studies show these particles can damage blood vessel walls, disrupt cholesterol processing, trigger inflammation, and promote blood clot formation, raising serious concerns about heart health.
Effect of Early-Life Exposure of Polystyrene Microplastics on Behavior and DNA Methylation in Later Life Stage of Zebrafish
Researchers exposed zebrafish embryos to polystyrene microplastics during early development and then assessed neurobehavioral effects later in life. The study found that early-life microplastic exposure caused lasting changes in behavior and DNA methylation patterns, suggesting that developmental exposure to microplastics may have long-term epigenetic consequences on neurodevelopment.
Microplastics cause hepatotoxicity in diabetic mice by disrupting glucolipid metabolism via PP2A/AMPK/HNF4A and promoting fibrosis via the Wnt/β‐catenin pathway
Researchers found that microplastic exposure caused liver damage in diabetic mice by disrupting the way the liver processes sugars and fats through specific cellular signaling pathways. The microplastics also promoted liver scarring through activation of a fibrosis-related pathway. The study suggests that individuals with existing metabolic conditions like diabetes may be particularly vulnerable to the harmful effects of microplastic accumulation in the body.