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61,005 resultsShowing papers similar to Integrative Analysis of Pharmacology and Transcriptomics Predicts Resveratrol Will Ameliorate Microplastics-Induced Lung Damage by Targeting Ccl2 and Esr1
ClearMicroplastic exposure and allergic rhinitis: Network toxicology, and molecular docking insights
Researchers used network toxicology and molecular docking approaches to investigate how microplastic exposure may contribute to allergic rhinitis. The study identified key molecular mediators through which microplastics may drive respiratory inflammation pathways, and found that resveratrol could potentially modulate these pathways, offering insights into the mechanisms linking microplastic exposure to allergic respiratory conditions.
Avaliação do efeito de citotoxicidade dos microplásticos na linhagem mamária humana MCF10A
Researchers assessed the cytotoxicity of microplastics on the non-tumoral human breast cell line MCF10A and explored whether the antioxidant resveratrol could mitigate those effects. The study found that microplastics negatively impacted cell viability and that resveratrol showed potential as a protective agent in the cellular context of MP exposure.
Assessing the toxicological effects of exposure to environmental pollutants PET-MPs on vascular diseases: insights from network toxicology, molecular docking, molecular dynamics, and experimental validation
Researchers used network toxicology, molecular docking, and cell experiments to investigate how PET microplastics may contribute to vascular diseases. They identified four core molecular targets and found that PET microplastics induced mitochondrial oxidative stress, increased reactive oxygen species, and promoted vascular smooth muscle cell death. The study provides initial molecular-level evidence that microplastic exposure may be a contributing factor in vascular damage and remodeling.
Intersection of microplastic toxicity targets and differentially expressed genes in allergic rhinitis.
Network analysis identified a set of genes that are both targeted by common microplastics (PE, PP, PVC, PS) and differentially expressed in allergic rhinitis, providing a molecular framework for investigating how microplastic exposure may contribute to nasal allergy pathogenesis.
Polyethylene terephthalate microplastics promote pulmonary fibrosis via AKT1, PIK3CD, and PIM1: A network toxicology and multi-omics analysis
Using computational toxicology and multi-omics analysis, researchers identified three key proteins (AKT1, PIK3CD, and PIM1) through which PET microplastics may promote pulmonary fibrosis, a serious scarring disease of the lungs. The microplastics appear to affect metabolic and inflammatory pathways in specific lung and immune cells. This study provides molecular evidence for how inhaled plastic particles from everyday items could contribute to chronic lung disease.
Protein-protein network analysis.
This study presents a protein-protein interaction network and LASSO regression analysis identifying key molecular targets through which microplastics may act in allergic rhinitis, using STRING database clustering and Genemama functional enrichment. The analysis identified three key gene targets and constructed a microplastic-target-pathway network to elucidate potential mechanistic pathways of microplastic-associated disease.
A particle of concern: explored and proposed underlying mechanisms of microplastic-induced lung damage and pulmonary fibrosis
This paper explores how inhaled microplastics may cause lung damage and scarring (pulmonary fibrosis) through several biological pathways. The research identifies signaling pathways that could be targeted for future treatments to reduce microplastic-induced lung damage. This is relevant to human health because people regularly breathe in airborne microplastic particles.
Synergistic pulmonary toxicity of resorcinol bis(diphenylphosphate) and microplastics: Integrated proteomics and metabolomics approach reveals oxidative stress-inflammatory crosstalk
Researchers exposed mice to the flame retardant resorcinol bis(diphenylphosphate) alone and in combination with polystyrene nanoplastics through inhalation. Using proteomics and metabolomics analysis, they found that co-exposure produced significantly worse lung damage than the flame retardant alone, through amplified oxidative stress and inflammatory signaling. The study reveals that nanoplastics can intensify the pulmonary toxicity of co-occurring environmental chemicals through synergistic mechanisms.
Effect and Mechanism of Fisetin on Patulin Induced Myocardial Damage Based on Network Pharmacology
This study used network pharmacology to investigate how fisetin, a plant compound, protects heart tissue from damage caused by patulin, a mycotoxin. While focused on cardiac pharmacology rather than microplastics, the research contributes to understanding how natural compounds can protect cells from toxic exposures.
Protective Effect of Resveratrol on Kidney Disease and Hypertension Against Microplastics Exposure in Male Juvenile Rats
Researchers investigated whether resveratrol, a natural plant compound, could protect young rats from kidney damage and high blood pressure caused by microplastic exposure. They found that microplastics elevated blood pressure and creatinine levels through oxidative stress, and that resveratrol treatment effectively prevented these effects. The study suggests resveratrol may offer protective benefits against organ damage linked to microplastic exposure, partly by improving gut microbiota balance.
The toxicological impact of PET-MPs exposure on atherosclerosis: insights from network toxicology, molecular docking, and machine learning
Researchers used network toxicology, molecular docking, and machine learning to identify how PET microplastics may promote atherosclerosis, narrowing 28 candidate targets to seven key genes and predicting interactions with atherosclerosis-relevant pathways including inflammation and lipid metabolism.
A computational framework for multi-scale data fusion in assessing the associations between micro- and nanoplastics and human hepatotoxicity
Researchers developed a computational toxicology framework integrating multi-source data and network analysis to map associations between micro- and nanoplastics and hepatotoxicity, identifying key molecular pathways through which MNPs may damage the liver, offering a scalable alternative to traditional in vivo testing.
Sesamin Protects Against Polystyrene Microplastics-Induced Lung Injury via Attenuating Bcl2-Mediated Apoptosis
Scientists found that sesamin, a natural compound found in sesame seeds, helped protect mice's lungs from damage caused by microplastics (tiny plastic particles we consume from food and water). The sesamin worked by preventing lung cells from dying and reducing harmful inflammation when exposed to these plastic particles. While more research is needed in humans, this suggests that eating sesame-based foods might help protect our lungs from the microplastics we're increasingly exposed to in our daily lives.
Evaluating the toxicological effects of PET-MPs exposure on atherosclerosis through integrated network toxicology analysis and experimental validation
Researchers used network toxicology analysis and laboratory experiments to investigate how polyethylene terephthalate microplastics may contribute to atherosclerosis. They identified several molecular targets and biological pathways through which these microplastics could promote plaque formation in blood vessels. The study provides preliminary evidence that a commonly encountered type of microplastic may interact with cardiovascular disease mechanisms, though further research is needed to confirm these findings.
Palliative potential of robinetin to avert polystyrene microplastics instigated pulmonary toxicity in rats
Researchers investigated whether the flavonoid compound robinetin could protect against lung damage caused by polystyrene microplastic exposure in rats. They found that robinetin supplementation reduced oxidative stress markers and inflammatory responses in lung tissue that had been damaged by microplastic ingestion. The study suggests that certain natural compounds may help mitigate some of the harmful effects of microplastic exposure on respiratory tissues.
Effect of microplastics deposition on human lung airways: A review with computational benefits and challenges
This review examines how microplastics deposited in human lungs can cause inflammation, oxidative stress, and reduced lung function. Because these tiny particles can reach deep into the lungs where oxygen enters the blood, they raise concerns about long-term respiratory disease and the possibility of spreading to other organs.
Multi-Omics Analysis Reveals the Toxicity of Polyvinyl Chloride Microplastics toward BEAS-2B Cells
Researchers used advanced gene and metabolite analysis to reveal how PVC microplastics damage human lung cells. Exposure altered the expression of 530 genes and nearly 4,000 metabolites, particularly disrupting fat metabolism pathways and activating inflammatory stress responses. These findings are important because airborne PVC microplastics are common in indoor and outdoor environments, and the study reveals specific biological pathways through which inhaled microplastics could contribute to lung disease.
Mechanism of circRNA_SMG6 mediating lung macrophage ECM degradation via miR-570-3p in microplastics-induced emphysema
In a rat study, inhaling polystyrene microplastics for 90 days caused lung damage resembling emphysema, including inflammation, thickened tissue walls, and enlarged air sacs. The microplastics triggered the breakdown of the structural support network in the lungs through a specific molecular pathway involving circular RNA. This research provides a mechanism by which breathing in microplastic particles could contribute to chronic lung disease in humans.
Inhaled microplastics and lung health: Immunopathological effects and disease implications
This review examines the molecular mechanisms by which inhaled microplastics damage lung health, focusing on oxidative stress, inflammation, and immune disruption. Researchers found that microplastics trigger reactive oxygen species production, deplete antioxidants, impair mitochondrial function, and compromise immune defenses in lung tissue. The evidence indicates that microplastics may also act as carriers for other toxic pollutants, amplifying respiratory health risks.
Integration of transcriptomics and metabolomics reveal cytotoxic mechanisms of Polyethylene terephthalate microplastics in BEAS-2B cells
Researchers exposed human lung cells to PET microplastics and used combined gene and metabolite analysis to uncover the mechanisms of toxicity. They found that the microplastics disrupted lipid metabolism and activated cell death pathways, reducing cell viability over time. The study suggests that inhaled PET microplastics could pose risks to respiratory health by triggering harmful molecular changes in lung tissue.
The impact of polyethylene terephthalate microplastics on the pathogenesis of atherosclerosis: Focusing on network toxicology and target gene detection
Researchers used network toxicology and gene analysis to investigate how PET microplastics may influence atherosclerosis, the buildup of plaque in arteries. They identified specific genes involved in inflammation and immune cell signaling that are affected by both PET exposure and atherosclerosis development. The study suggests that microplastic exposure could worsen cardiovascular disease through shared inflammatory pathways.
Reformulating asthma therapy through nano-phytomedicine: Insights into lung health and microplastic exposure
This review examines the use of nanotechnology-based phytomedicine formulations to improve asthma treatment, while also exploring how microplastic inhalation contributes to lung inflammation and airway dysfunction, framing microplastic exposure as a key driver of rising asthma prevalence.
Tracing Microplastics in the Human Body: From Detection to Disease Mechanisms
This review traces the detection of microplastics across multiple human tissues — from nasal lavage and bronchoalveolar fluid to blood and lung tissue — and examines the disease mechanisms linking plastic particle accumulation to respiratory, cardiovascular, and other systemic health effects.
Resveratrol Butyrate Esters Reduce Hypertension in a Juvenile Rat Model of Chronic Kidney Disease Exacerbated by Microplastics
Researchers found that resveratrol butyrate esters reduced high blood pressure in young rats that had both chronic kidney disease and microplastic exposure. The protective effects worked by improving nitric oxide levels, regulating the body's blood pressure control system, and positively shifting gut bacteria composition. The study suggests that certain natural compounds may help counteract the cardiovascular harm associated with microplastic exposure.