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61,005 resultsShowing papers similar to Autophagy affects hepatic fibrosis progression by regulating macrophage polarization and exosome secretion
ClearExosome‐derived miR ‐142‐5p from liver stem cells improves the progression of liver fibrosis by regulating macrophage polarization through CTSB
This paper is not about microplastics; it investigates how exosome-derived microRNA from liver stem cells affects liver fibrosis progression through macrophage regulation.
A bibliometric analysis of autophagy in lung diseases from 2012 to 2021
This bibliometric analysis maps autophagy research in lung diseases from 2012 to 2021, identifying key research hotspots, collaboration networks, and emerging trends linking autophagy mechanisms to various pulmonary conditions.
Reversibility of Renal Fibrosis Induced by Exposure to Polystyrene Nanoplastics: The Dual Role of Lysosomes
Researchers exposed mice to 100 nm and 500 nm polystyrene nanoplastics and examined renal fibrosis, lysosomal function, and autophagy pathways. PS100 induced more pronounced kidney fibrosis than PS500 by impairing lysosomal degradation and disrupting autophagic flux; notably, fibrosis partially reversed after cessation of exposure, suggesting some reversibility in nanoplastic-induced kidney injury.
Acute Endoplasmic Reticulum Stress Induces Inflammation Reaction, Complement System Activation, and Lipid Metabolism Disorder of Piglet Livers: A Proteomic Approach
Researchers used piglet liver models to show that acute endoplasmic reticulum stress triggers a cascade of inflammation, complement system activation, and lipid metabolism disruption, providing proteomic insights relevant to understanding stress-related liver disease mechanisms.
Non-parenchymal cells: key targets for modulating chronic liver diseases
This review examines how specialized non-parenchymal cells in the liver drive chronic liver diseases like fatty liver disease, fibrosis, and cirrhosis through inflammation and scarring. While not directly about microplastics, these are the same cell types and disease pathways that microplastics and nanoplastics have been shown to activate when they accumulate in liver tissue. Understanding these mechanisms helps explain how environmental pollutants like microplastics could contribute to the growing burden of chronic liver disease.
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.
HIF-PHI regulates the STING-TBK1-IRF3 signaling pathway and mediates macrophage polarization to alleviate renal interstitial fibrosis
Researchers investigated how hypoxia-inducible factor proline hydroxylase inhibitors affect kidney fibrosis by targeting macrophage behavior through the STING-TBK1-IRF3 signaling pathway. They found that these inhibitors promoted a shift from inflammatory to anti-inflammatory macrophage states, reducing fibrosis progression in both cell and animal models. The study advances understanding of immune-mediated tissue damage, a process also relevant to how the body responds to foreign particles like microplastics.
FGFR2-regulated cytoskeletal rearrangement disturbs autophagy flux induced by polystyrene nanoplastics
Researchers found that polystyrene nanoparticles activate the cell-surface receptor FGFR2 in liver cells, triggering cytoskeletal rearrangement that blocks the normal autophagy pathway — the cell's waste-removal system — leading to mitochondrial and lysosomal dysfunction and identifying a previously unknown molecular mechanism for nanoplastic cellular toxicity.
ReversibilityofRenal Fibrosis Induced by Exposureto Polystyrene Nanoplastics: The Dual Role of Lysosomes
This mouse study investigated whether kidney fibrosis caused by low-level polystyrene nanoplastics (100 nm and 500 nm) is reversible, finding that 100 nm particles caused more severe fibrosis and that lysosomes played a dual role — initially impairing autophagy flux to promote fibrosis, then recovering to facilitate partial reversal after exposure ended.
Impact of microplastics and nanoplastics on liver health: Current understanding and future research directions
This review summarizes what scientists know about how micro- and nanoplastics affect the liver, which is one of the first organs exposed because it processes everything absorbed from the gut. The particles trigger oxidative stress, disrupt energy metabolism, cause cell death, and promote inflammation, and may contribute to conditions like fatty liver disease and liver fibrosis. The paper also highlights how plastics can disturb the gut microbiome, which communicates with the liver through the gut-liver axis and may amplify liver damage.
Biological Modulation of Autophagy by Nanoplastics: A Current Overview
This review examines how nanoplastics interfere with autophagy, the cell's natural recycling and cleanup process. While cells initially activate autophagy to deal with nanoplastic particles, prolonged exposure can overwhelm this system, leading to cell damage and death. Understanding this process is important because it may explain how long-term nanoplastic exposure contributes to tissue damage and disease in humans.
International consensus guidelines for the definition, detection, and interpretation of autophagy-dependent ferroptosis
This scientific review provides guidelines for understanding a specific type of cell death called autophagy-dependent ferroptosis, where cells essentially digest their own protective components and then die from iron-driven damage. While not directly about microplastics, this process is relevant because microplastics and nanoplastics have been shown to trigger oxidative stress and iron-related cell damage in tissues. Understanding these cell death pathways helps researchers assess how plastic particle exposure could harm organs like the liver, brain, and lungs.
Redox Biology and Liver Fibrosis
This review explores how disrupted redox balance in the liver contributes to the development and progression of hepatic fibrosis across various chronic liver diseases. Researchers describe how persistent damage to liver cells triggers overproduction of reactive species, which in turn activate specific signaling pathways that drive scar tissue formation. The study identifies several redox-dependent pathways as potential therapeutic targets for slowing or preventing liver fibrosis.
Polystyrene nanoplastics induce lipophagy via the AMPK/ULK1 pathway and block lipophagic flux leading to lipid accumulation in hepatocytes
Polystyrene nanoplastics caused fat to accumulate in human liver cells by disrupting the normal fat-breakdown process called lipophagy. The nanoplastics triggered the cells to start digesting fat droplets but then blocked the final cleanup step by damaging the cell's recycling centers (lysosomes), leaving excess fat trapped inside. This newly identified mechanism helps explain how nanoplastic exposure could contribute to fatty liver disease.
Advances in the regulatory mechanisms of mTOR in necroptosis
This review explores how the mTOR signaling pathway regulates necroptosis, a form of programmed cell death distinct from apoptosis. Researchers describe multiple mechanisms through which mTOR influences cell death, including direct regulation of key necroptosis proteins, indirect effects through autophagy, and modulation of reactive oxygen species. The study highlights that mTOR can both promote and inhibit necroptosis depending on the context, making it a complex but promising therapeutic target.
Polystyrene microplastics-induced macrophage extracellular traps contributes to liver fibrotic injury by activating ROS/TGF-β/Smad2/3 signaling axis
In a mouse study, polystyrene microplastics caused liver scarring (fibrosis) by triggering immune cells called macrophages to release web-like traps that promoted inflammation. Smaller microplastic particles caused more severe liver damage than larger ones, and the damage involved a specific signaling pathway (ROS/TGF-beta/Smad2/3) that drives tissue scarring. This research reveals a new mechanism by which microplastics may contribute to chronic liver disease.
Autophagic response of intestinal epithelial cells exposed to polystyrene nanoplastics
Researchers found that polystyrene nanoplastics accumulate in the cytoplasm of intestinal epithelial cells, impairing autophagic flux and triggering an autophagic stress response confirmed in both cell and animal models.
Drosophila as a Robust Model System for Assessing Autophagy: A Review
This review explores how the fruit fly Drosophila melanogaster serves as a powerful research model for studying autophagy, the cellular recycling process that plays roles in aging, immune response, and disease. Researchers describe the genetic tools and techniques available in Drosophila that allow detailed investigation of autophagy mechanisms in a living organism. The study highlights that insights from fruit fly research continue to advance our understanding of how autophagy functions in more complex organisms, including humans.
The impact of nanomaterials on autophagy across health and disease conditions
Researchers examined how nanomaterials — including nanoplastics — interact with autophagy, the cell's internal recycling and cleanup system. Depending on the type and dose, nanoplastics can either trigger helpful cellular defense responses or push cells toward self-destruction, a dual nature that has important implications for both environmental health and the design of nanomaterial-based medicines.
Polystyrene nanoplastics exacerbate dibutyl phthalate-induced liver fibrosis through PDGFRα-dependent hepatic stellate cell activation
Researchers found that polystyrene nanoplastics worsen liver fibrosis caused by dibutyl phthalate, a common plasticizer, through activation of hepatic stellate cells via the PDGFRalpha signaling pathway. The study suggests that nanoplastics act as environmental carriers that facilitate cellular uptake of harmful plasticizers, amplifying their toxic effects on liver tissue.
Targeting Regulated Cell Death Pathways in COPD: Mechanisms and Therapeutic Strategies
This review examines how multiple regulated cell death pathways — including apoptosis, necroptosis, pyroptosis, ferroptosis, and autophagy — contribute to chronic obstructive pulmonary disease progression and discusses these pathways as potential therapeutic targets.
Microplastic exposure aggravates pneumococcus-induced inflammation in macrophages by activating ferroptosis
Researchers investigated how microplastic exposure affects the immune response of macrophages to pneumococcal (Streptococcus pneumoniae) infection. They found that microplastics impaired macrophage phagocytosis, inhibited bacterial clearance, and amplified inflammation by activating ferroptosis and promoting M1 macrophage polarization through PI3K/Akt and MAPK/ERK signaling pathways. The study suggests that microplastic exposure may worsen bacterial lung infections by compromising immune cell function.
Proteomics reveals that nanoplastics with different sizes induce hepatocyte apoptosis in mice through distinct mechanisms involving mitophagy dysregulation and cell cycle arrest
Mice fed diets containing 100 nm polystyrene nanoplastics for 180 days showed more hepatocyte apoptosis than those fed 500 nm particles, with proteomic analysis revealing size-dependent mechanisms involving Pdcd2l-mediated cell cycle arrest and distinct mitophagy dysregulation pathways.
Nanoplastic propels diet-induced NAFL to NASH via ER-mitochondrial tether-controlled redox switch
Researchers investigated how nanoplastic exposure may accelerate the progression of diet-induced fatty liver conditions in animal models. The study found that nanoplastics disrupted the connections between the endoplasmic reticulum and mitochondria, triggering oxidative stress responses that worsened liver inflammation and damage.