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Papers
9 resultsShowing papers from Tongren Hospital
ClearFerroptosis 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.
Toxicological effects of microplastics in renal ischemia–reperfusion injury
Researchers studied how microplastic exposure affects kidney injury and recovery in a mouse model of reduced blood flow to the kidneys. They found that microplastics worsened kidney damage by triggering inflammatory responses and disrupting cellular repair processes. The study suggests that microplastic accumulation in the body may increase vulnerability to kidney complications.
Transcriptome-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.
A novel tiRNA-Glu-CTC induces nanoplastics accelerated vascular smooth muscle cell phenotypic switching and vascular injury through mitochondrial damage
Researchers discovered that nanoplastic exposure activates a specific small RNA molecule called tiRNA-Glu-CTC, which accelerates harmful changes in blood vessel smooth muscle cells. This molecular mechanism caused mitochondrial damage and promoted the kind of cell behavior associated with vascular injury and disease. The study identifies a new biological pathway through which nanoplastics may contribute to cardiovascular harm.
Polystyrene nanoplastics induce vascular stenosis via regulation of the PIWI-interacting RNA expression profile
Researchers exposed mice to polystyrene nanoplastics and found evidence that the particles can contribute to the narrowing of blood vessels, known as vascular stenosis. The nanoplastics triggered changes in gene expression related to small RNA molecules called PIWI-interacting RNAs, which appear to play a role in the vascular damage. The study suggests that nanoplastic exposure may pose risks to cardiovascular health through previously unrecognized molecular pathways.
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.
N6-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 in COPD Alters the Immune Microenvironment: Implications for Tumor-Promoting Inflammation
Researchers used single-cell RNA sequencing to analyze how microplastic exposure affects the lung immune environment in mice with COPD. They found that microplastics worsened inflammation, increased immune cell exhaustion, and reduced the population of cells critical for lung repair, creating conditions that may be more favorable for tumor development. The study suggests that microplastic exposure may intensify the already elevated cancer risk associated with COPD by promoting a tumor-permissive immune environment.
Multi-omics analysis reveals size-dependent toxicity and vascular endothelial cell injury induced by microplastic exposurein vivoandin vitro
Researchers used multi-omics analysis to reveal that microplastics cause size-dependent toxicity and injury to vascular endothelial cells both in vivo and in vitro, identifying the vascular system as a previously understudied target of microplastic exposure.