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61,005 resultsShowing papers similar to Caffeic Acid Phenethyl Ester Ameliorates Pulmonary Fibrosis by Inhibiting Epithelial-Mesenchymal Transition via the Sirt1/PGC-1α/Mitochondrial Axis
ClearHesperidin inhibits tobacco smoke‑induced pulmonary cell proliferation and EMT in mouse lung tissues via the p38 signaling pathway
Researchers found that hesperidin, a natural flavonoid compound, inhibits tobacco smoke-induced lung cell proliferation and epithelial-mesenchymal transition in mice by suppressing the p38 signaling pathway, suggesting a potential role in reducing lung cancer risk.
Ethanol Extract of Rosa rugosa Ameliorates Acetaminophen-Induced Liver Injury via Upregulating Sirt1 and Subsequent Potentiation of LKB1/AMPK/Nrf2 Cascade in Hepatocytes
Researchers prepared an ethanol extract from Rosa rugosa flower buds and found it significantly reduced liver damage caused by acetaminophen overdose in both cell and mouse models. The extract worked by activating the Sirt1 protein and boosting a protective signaling pathway that counters oxidative stress in liver cells. The study suggests Rosa rugosa extract may have potential as a natural intervention for drug-induced liver injury.
Coal dust nanoparticles induced pulmonary fibrosis by promoting inflammation and epithelial-mesenchymal transition via the NF-κB/NLRP3 pathway driven by IGF1/ROS-mediated AKT/GSK3β signals
Researchers investigated how coal dust nanoparticles trigger lung scarring (pulmonary fibrosis) in coal miners, identifying a molecular chain reaction where nanoparticles activate the IGF1 signaling pathway, generate damaging reactive oxygen species, and ultimately drive inflammation and tissue remodeling. The study pinpoints specific drug targets that could potentially prevent or treat the lung disease that affects millions of miners worldwide.
Senescence in Pulmonary Fibrosis: Between Aging and Exposure
This review examines the role of cellular senescence in pulmonary fibrosis, considering both natural aging processes and environmental exposures such as air pollutants and particulates. It discusses how genomic instability, telomere shortening, and other hallmarks of senescence interact with fibrotic lung disease development in an aging global population.
The interplay of ferroptosis and oxidative stress in pulmonary fibrosis: from mechanisms to treatment
This research review summarizes how a specific type of cell death called ferroptosis may contribute to pulmonary fibrosis, a serious lung disease where scar tissue builds up and makes breathing difficult. Scientists have found that when cells die from iron buildup and damage from harmful molecules, it can worsen lung scarring, but drugs that block this process show promise in animal studies. Understanding this connection could lead to new treatments for people with pulmonary fibrosis, though more research is needed to make sure these potential medicines are safe and effective in humans.
Quercetin alleviates cyclophosphamide-induced premature ovarian insufficiency in mice by reducing mitochondrial oxidative stress and pyroptosis in granulosa cells
Researchers found that quercetin, a natural plant compound, protected mouse ovaries from chemotherapy-induced damage by reducing harmful oxidative stress in mitochondria and suppressing a form of inflammatory cell death called pyroptosis, suggesting it could help preserve fertility in patients undergoing cancer treatment.
Pharmacological Inhibition of STING/TBK1 Signaling Attenuates Myeloid Fibroblast Activation and Macrophage to Myofibroblast Transition in Renal Fibrosis
Researchers found that pharmacological inhibition of the STING/TBK1 signaling pathway attenuated renal fibrosis in mice by reducing myeloid fibroblast activation and macrophage-to-myofibroblast transition, identifying a potential therapeutic target for chronic kidney disease.
The Effect of Modern Lifestyle on Cardiovascular Health
Researchers investigated how PET microplastics affect vascular endothelial function and tested whether Sirtuin 1 (SIRT1) could provide protection against PET-induced damage in human umbilical vein endothelial cells. PET exposure impaired endothelial function and increased inflammation, while SIRT1 activation partially restored vascular health markers.
Mitochondrial Dysfunction and Nanocarrier-Based Treatments in Chronic Obstructive Pulmonary Disease (COPD)
This review examines how mitochondrial dysfunction contributes to the development and progression of chronic obstructive pulmonary disease. Researchers highlight emerging nanocarrier-based drug delivery systems designed to target mitochondrial dysfunction in lung tissue. The study suggests these novel nanoparticle approaches, while still in early clinical stages, represent a promising direction for future treatments.
Toxic effects of nanoplastics with different sizes and surface charges on epithelial-to-mesenchymal transition in A549 cells and the potential toxicological mechanism
Researchers exposed human lung cells to polystyrene nanoplastics of different sizes and surface charges and found they triggered a process called epithelial-to-mesenchymal transition, which is associated with the early stages of lung fibrosis. Smaller particles and those with positive surface charges caused the strongest effects, activating oxidative stress and inflammatory pathways. The study suggests that inhaled nanoplastics could contribute to respiratory health risks by promoting tissue scarring in the lungs.
Artemisia gmelinii Extract Attenuates Particulate Matter-Induced Neutrophilic Inflammation in a Mouse Model of Lung Injury
Researchers tested whether Artemisia gmelinii extract could reduce particulate matter-induced neutrophilic lung inflammation in mice, finding that it significantly decreased inflammatory chemokines, neutrophil extracellular trap formation, and total inflammatory cell counts in bronchoalveolar lavage fluid. The plant extract shows potential as a natural therapeutic agent for managing particulate matter-induced respiratory inflammation.
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.
Intratracheal Administration of Polystyrene Micro(nano)plastics with a Mixed Particle Size Promote Pulmonary Fibrosis in Rats by Activating TGF-β1 Signaling and Destabilizing Mitochondrial Dynamics and Mitophagy in a Dose- and Time-Dependent Manner.
SD rats exposed to mixed polystyrene micro(nano)plastics via intratracheal administration at escalating doses over time developed pulmonary fibrosis and mitochondrial dysfunction, with severity linked to dose. The findings demonstrated a clear biological pathway connecting inhaled microplastic exposure to lung injury.
Integrative Analysis of Pharmacology and Transcriptomics Predicts Resveratrol Will Ameliorate Microplastics-Induced Lung Damage by Targeting Ccl2 and Esr1
Researchers used pharmacology network analysis and transcriptomics to predict that resveratrol may help mitigate lung damage caused by microplastic exposure. They identified two key molecular targets, Ccl2 and Esr1, through which resveratrol could exert protective effects. The study offers a new perspective on potential approaches to addressing microplastic-induced lung injury, though further experimental validation is needed.
5-methoxyindole-3-carboxaldehyde attenuates alveolar type II epithelial cell senescence induced by exposure to polystyrene microplastics in pulmonary fibrosis via PI3K/AKT/mTOR signaling pathway
Researchers found that polystyrene microplastic exposure in mice disrupted airway microbial communities and promoted lung fibrosis through metabolic changes. The study identified a microbial metabolite called 5-methoxyindole-3-carboxaldehyde (5-MC) that was reduced by microplastic-induced dysbiosis and could attenuate lung cell aging through the PI3K/AKT/mTOR signaling pathway. The findings suggest that microplastics may drive pulmonary fibrosis by disrupting the balance of protective metabolites produced by airway microbes.
Dimethyl Bisphenolate Ameliorates Carbon Tetrachloride-Induced Liver Injury by Regulating Oxidative Stress-Related Genes
Researchers synthesized a novel compound called dimethyl bisphenolate and tested its ability to protect against chemically induced liver injury in rats and cell models. They found that the compound significantly reduced liver damage markers and oxidative stress in a dose-dependent manner, with effects comparable to the established liver protectant silymarin. The study suggests that dimethyl bisphenolate may help protect liver cells by regulating oxidative stress pathways and reducing cell death.
Protective Effect of Astragaloside IV against Cadmium-Induced Damage on Mouse Renal Podocytes (MPC5)
This paper is not about microplastics; it investigates how the plant compound Astragaloside IV protects kidney cells from cadmium-induced damage, examining mitochondrial and autophagy pathways.
CHEMOPREVENTIVE POTENTIAL OF ALCOHOLIC EXTRACT OF A POLYHERBAL ( Phyllanthus amarus, Euphorbia hirta and Azadirachta indica) RECIPE AGAINST BENZO(a)PYRENE INDUCED LUNG CARCINOGENESIS IN ALBINO MICE
Researchers assessed the chemopreventive potential of an alcoholic extract of a polyherbal preparation including Phyllanthus amarus in a precancerous lesion model, measuring effects on biomarkers of oxidative stress and inflammation. The herbal extract reduced key biomarkers compared to untreated controls, supporting further investigation of plant-derived compounds as adjuncts in cancer chemoprevention.
Melatonin prevents allergic airway inflammation in epicutaneously sensitized mice
This study demonstrated that melatonin administration suppressed NF-kB-mediated allergic airway inflammation in epicutaneously sensitized mice, suggesting that antioxidant treatment may be a viable strategy for preventing progression of atopic disease from skin sensitization to lung inflammation.
Polyethylene Micro/Nanoplastics Exposure Induces Epithelial–Mesenchymal Transition in Human Bronchial and Alveolar Epithelial Cells
When human lung cells were exposed to polyethylene micro- and nanoplastics (the most common type of plastic pollution), the cells underwent a transformation called epithelial-mesenchymal transition, where they changed shape, reorganized their internal structure, and gained increased ability to migrate. This cellular change is a known early step in both lung fibrosis and cancer development, suggesting that inhaling polyethylene plastics could contribute to serious lung diseases.
Tea Polyphenols Mitigate TBBPA-Induced Renal Injury Through Modulation of ROS-PI3K/AKT-NF-κB Signalling in Carp (Cyprinus carpio)
Researchers found that tea polyphenols, the beneficial compounds in tea, helped protect carp kidneys from damage caused by the flame retardant chemical TBBPA. The tea compounds reduced oxidative stress, inflammation, and cell death in kidney tissue by modulating key signaling pathways. The study suggests that natural antioxidants like those found in tea may help mitigate some of the harmful effects of environmental chemical pollutants on aquatic organisms.
Sciadopitysin attenuates paraquat induced renal toxicity by modulating Nrf2/Keap-1 pathway in male albino rats
Researchers investigated whether the plant compound sciadopitysin could protect against kidney damage caused by the herbicide paraquat in rats. They found that sciadopitysin significantly reduced oxidative stress and inflammation in the kidneys by activating the Nrf2/Keap-1 protective pathway. The study suggests that natural biflavonoid compounds may help mitigate organ damage from toxic environmental chemical exposures.
Icariin improves cardiac function and remodeling via the TGF-β1/Smad signaling pathway in rats following myocardial infarction
This paper is not about microplastic pollution. It studies the effects of icariin, a plant-derived compound, on cardiac function and tissue remodeling in rats after heart attacks, finding that it works through the TGF-beta1/Smad signaling pathway.
Inhaled tire-wear microplastic particles induced pulmonary fibrotic injury via epithelial cytoskeleton rearrangement
Researchers investigated the health effects of inhaling tire-wear microplastic particles in mice and found that exposure caused lung fibrosis and restricted breathing function. The study identified that the particles triggered rearrangement of the structural framework in lung cells, leading to scarring and tissue damage through epigenetic mechanisms. These findings suggest that airborne tire-wear particles, a common but understudied pollutant, may pose a significant risk to respiratory health.