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61,005 resultsShowing papers similar to N6-methyladenosine methylation mediates non-coding RNAs modification in microplastic-induced cardiac injury
ClearTranscriptome-wide m6A modification mediates cardiotoxicity in mice after chronic exposure to microplastics
Researchers exposed mice to microplastics and examined the resulting heart tissue damage and changes in gene regulation through a chemical modification called m6A methylation. They found that microplastic exposure caused cardiac inflammation, fibrosis, and increased lipid accumulation, along with widespread changes in m6A methylation patterns across the transcriptome. The study suggests that microplastics may contribute to heart tissue damage through epigenetic modifications that alter gene expression.
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.
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.
N6-methyladenosine RNA methylation regulates microplastics-induced cell senescence in the rainbow trout liver
Rainbow trout exposed to microplastics at 500 µg/L for two weeks accumulated plastic particles in their livers, which triggered oxidative stress, liver tissue damage, and — importantly — premature cell ageing (senescence) driven by changes in RNA regulation. Specifically, microplastics disrupted a molecular "reader" system (m6A RNA methylation) that normally controls cell proliferation and growth. This pathway-level finding is significant because cellular senescence is associated with tissue degeneration and disease, suggesting microplastic exposure may have long-term liver health consequences in fish — and potentially in other vertebrates.
A study on the roles of long non-coding RNA and circular RNA in the pulmonary injuries induced by polystyrene microplastics
Researchers exposed rats to polystyrene microplastics through the airways and found evidence of lung tissue damage, including destroyed air sacs and inflammation. The study identified changes in the activity of long non-coding RNAs and circular RNAs, types of genetic regulators that may help explain how microplastics cause lung injury at the molecular level. These findings provide new insight into the biological mechanisms behind potential respiratory harm from inhaling microplastic particles.
Whole transcriptome sequencing analysis revealed key RNA profiles and toxicity in mice after chronic exposure to microplastics
Researchers examined the long-term effects of environmental levels of microplastics on mice given polystyrene particles in drinking water for 180 days. Whole transcriptome analysis revealed significant changes in RNA expression profiles, with biochemical and histopathological examination showing organ-level impacts. The study suggests that chronic exposure to microplastics at environmentally relevant concentrations can alter key molecular signaling pathways in mammals.
Nanoplastics: Focus on the role of microRNAs and long non-coding RNAs
This review explored how nanoplastics may affect gene expression through epigenetic mechanisms, focusing on their potential to alter microRNA and long non-coding RNA regulation, which could contribute to chronic diseases including cancer.
Dynamic non-coding RNA biomarker reveals lung injury and repair induced by polystyrene nanoplastics
Researchers found that mice and lung organoids (lab-grown mini-organs) repeatedly exposed to polystyrene nanoplastics suffered lung tissue damage, impaired repair processes, and changes in non-coding RNA molecules that could serve as early warning biomarkers for nanoplastic-induced lung injury.
Paternal Microplastic Exposure Alters Sperm Small Noncoding RNAs and Affects Offspring Metabolic Health in Mice
Researchers found that paternal microplastic exposure in mice altered sperm small noncoding RNA profiles and had sex-specific effects on offspring metabolic health, including altered body composition and worsened insulin resistance in female offspring fed a high-fat diet. The study suggests that microplastic exposure may cause intergenerational health effects transmitted through epigenetic changes in sperm.
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.
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.
Exposure to Polypropylene Microplastics Causes Cardiomyocyte Apoptosis Through Oxidative Stress and Activation of the MAPK‐Nrf2 Signaling Pathway
Researchers found that polypropylene microplastics caused heart muscle cell death in both mice and lab-grown cells by triggering oxidative stress and activating specific cell damage pathways. Mice exposed to higher concentrations showed visible heart tissue damage and inflammation. This study is one of the first to demonstrate that microplastic exposure can directly harm the heart, raising concerns about cardiovascular effects in people exposed to microplastics.
Nanoplastics causes heart aging/myocardial cell senescence through the Ca2+/mtDNA/cGAS-STING signaling cascade
Researchers discovered that nanoplastics can cause heart aging by entering heart muscle cells and triggering a chain reaction: they damage mitochondria (the cell's energy source), which leaks DNA into the cell, activating an immune alarm system called the cGAS-STING pathway. This is the first study to reveal how long-term nanoplastic exposure could accelerate heart aging, raising concerns about the cardiovascular effects of plastic pollution.
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.
Emerging Roles for DNA 6mA and RNA m6A Methylation in Mammalian Genome
This review explores recently discovered chemical modifications on DNA and RNA molecules, specifically methylation at the sixth position of adenine, and their roles in regulating gene activity in mammals. Researchers found that these modifications are particularly enriched in brain tissue and may influence neurological development and disease. The study summarizes current detection methods and highlights significant gaps in understanding how these molecular markers function in mammalian biology.
Supplemental Data for "Paternal microplastic exposure alters sperm small non-coding RNAs and affects offspring metabolic health in mice"
This dataset provides supplemental data for a study examining how paternal microplastic exposure in mice alters small non-coding RNAs in sperm, with downstream effects on offspring metabolic health.
Epigenetic Modifications and Gene Expression Alterations in Plants Exposed to Nanomaterials and Nanoplastics: The Role of MicroRNAs, lncRNAs and DNA Methylation
This review examines how nanomaterials and nanoplastics alter plant gene expression through epigenetic mechanisms, focusing on changes in microRNA, long non-coding RNA, and DNA methylation patterns that could disrupt normal plant development and stress responses.
PVC nanoplastics impair cardiac function via lysosomal and mitochondrial dysfunction
Researchers found that PVC nanoplastics damaged heart cells by disrupting two critical cellular structures: lysosomes (the cell's recycling system) and mitochondria (the cell's energy producers). The nanoplastics caused lysosomes to become leaky and mitochondria to malfunction, leading to heart cell injury and impaired cardiac function. This study is concerning because PVC is one of the most common plastics, and the findings suggest that nanoplastic exposure could contribute to heart disease.
Identification of microRNA-mRNA regulatory network associated with microplastic exposure in Mytilus galloprovincialis
Scientists identified specific microRNA-mRNA regulatory networks in Mediterranean mussels that are altered by microplastic exposure, revealing how plastic pollution affects gene regulation at the molecular level. The study found that microplastics disrupt biological pathways related to development, growth, and reproduction in these filter-feeding organisms. Since mussels are widely consumed as seafood, the findings also raise concerns about microplastics entering the human food chain.
Profiling of lincRNAs and differential regulatory mechanisms in response to nanoplastic toxicity at environmentally relevant concentrations in Caenorhabditis elegans
Researchers investigated how polystyrene nanoplastics at environmentally relevant concentrations affect long noncoding RNA expression in the model organism C. elegans. The study identified specific regulatory mechanisms involving lncRNAs in the toxic response to nanoplastic exposure, providing new insights into the molecular pathways through which nanoplastics may harm living organisms.
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.
Additional file 1 of Single-cell RNA-seq analysis decodes the kidney microenvironment induced by polystyrene microplastics in mice receiving a high-fat diet
Researchers used single-cell RNA sequencing to decode kidney microenvironmental changes induced by polystyrene microplastics in mice fed a high-fat diet, characterizing mural cell and mesangial cell heterogeneity, DEG profiles, and pathway enrichment in affected renal tissue.
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.
Nanoplastics induces arrhythmia in human stem-cells derived cardiomyocytes
Researchers exposed human cardiomyocytes derived from stem cells to nanoplastic particles and observed dose-dependent uptake, oxidative stress, and arrhythmias developing by day seven. Complementary experiments in mice revealed that nanoplastics disrupted RNA processing and protein folding in heart tissue, leading to cellular stress and impaired electrical signaling. The study provides evidence that nanoplastic exposure may pose direct risks to heart rhythm and function.