We can't find the internet
Attempting to reconnect
Something went wrong!
Hang in there while we get back on track
Papers
61,005 resultsShowing papers similar to HIF-PHI regulates the STING-TBK1-IRF3 signaling pathway and mediates macrophage polarization to alleviate renal interstitial fibrosis
ClearPharmacological 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.
Polystyrene microplastics facilitate renal fibrosis through accelerating tubular epithelial cell senescence
Mice exposed to polystyrene microplastics at doses relevant to human exposure developed kidney inflammation and scarring (fibrosis) within 28 days. The microplastics caused kidney tube cells to age prematurely, triggering a chain reaction that activated scar-forming cells through a specific signaling pathway. This study provides evidence that microplastic exposure could contribute to chronic kidney damage in people.
Macrophage Migration Inhibitory Factor (MIF) suppresses mitophagy through disturbing the protein interaction of PINK1-Parkin in sepsis-associated acute kidney injury
This biomedical study investigated how an inflammatory protein (MIF) suppresses the protective cell process of mitophagy in sepsis-related kidney injury. This is a medical research paper on kidney disease mechanisms with no connection to environmental microplastics.
PS-MPs promotes the progression of inflammation and fibrosis in diabetic nephropathy through NLRP3/Caspase-1 and TGF-β1/Smad2/3 signaling pathways.
In a mouse model of diabetic nephropathy, polystyrene microplastic exposure worsened kidney inflammation and fibrosis by activating the NLRP3/Caspase-1 and TGF-beta1/Smad2/3 signaling pathways, suggesting microplastics may accelerate progression of this common diabetic complication.
Autophagy affects hepatic fibrosis progression by regulating macrophage polarization and exosome secretion
This study found that autophagy regulates hepatic fibrosis progression by controlling macrophage polarization and exosome secretion, which in turn modulates hepatic stellate cell activation.
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.
Polystyrene microplastics exacerbate experimental chronic kidney disease via inflammatory and oxidative pathways involving NF-κB, ERK/p38 MAPK, and sirtuin-1
Researchers examined the effects of polystyrene microplastics on mice with chronic kidney disease and found that microplastic exposure worsened kidney dysfunction, inflammation, and tissue scarring. Even in healthy mice, microplastics reduced kidney filtration and increased markers of kidney damage. The study suggests that microplastic exposure may aggravate existing kidney conditions through inflammatory and oxidative stress pathways.
Polystyrene-nanoplastics-induced unfolded protein response in monocyte-derived macrophages mediates pulmonary fibrosis via oxidative-stress-dependent IL-6 secretion
Researchers found that inhaled polystyrene nanoplastics promote pulmonary fibrosis by activating macrophages through a PERK/oxidative stress/IL-6 signaling cascade — in which nanoplastics trigger an unfolded protein response (a cellular stress reaction) that drives IL-6 secretion and transforms fibroblasts into scar-forming cells — identifying IL-6 as a potential therapeutic target.
STS Protects Diabetic Glomerular Vascular Endothelial Barrier by Ameliorating EPC Dysfunction: Targeting RAGE-TXNIP-NLRP3 Inflammasome Pathway
This study investigated how a compound called STS (Sodium Tanshinone IIA Sulfonate) protects kidney blood vessels in diabetic kidney disease by targeting an inflammatory pathway. STS helped repair endothelial progenitor cells that are damaged by diabetes, reducing kidney injury. This paper is focused on a therapeutic mechanism in diabetes and is not directly related to microplastics.
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.
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.
Chronic exposure to polystyrene microplastics induces renal fibrosis via ferroptosis
Mice exposed to polystyrene microplastics in their drinking water for six months developed kidney scarring (fibrosis) driven by a type of cell death called ferroptosis. The microplastics triggered iron-dependent damage in kidney cells, which then released signals causing surrounding tissue to scar over. This long-term study reveals a new mechanism by which chronic microplastic exposure could lead to progressive kidney disease in humans.
Polystyrene microplastics induce pulmonary fibrosis by promoting alveolar epithelial cell ferroptosis through cGAS/STING signaling
Researchers found that mice exposed to polystyrene microplastics through their noses developed lung scarring (fibrosis) because the plastic particles triggered a form of cell death called ferroptosis, involving iron buildup and cell damage in lung tissue. Blocking the specific signaling pathway responsible (cGAS/STING) reduced the lung damage, pointing to a potential treatment approach if microplastic-related lung disease becomes a clinical concern.
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.
Sotagliflozin prevents acute kidney injury by suppressing oxidative stress, inflammation, and apoptosis in renal ischemia/reperfusion rat model
This study found that sotagliflozin, a dual SGLT1/2 inhibitor, protects against acute kidney injury in rats by reducing oxidative stress, inflammation, and cell death in a renal ischemia/reperfusion model. While not directly about microplastics, the study is relevant to understanding kidney protection mechanisms, as microplastics have been detected in kidney tissue and may contribute to renal inflammation.
Polystyrene microplastics induced oxidative stress, inflammation and necroptosis via NF-κB and RIP1/RIP3/MLKL pathway in chicken kidney
Researchers exposed chickens to different doses of polystyrene microplastics for six weeks to study kidney damage. The study found that microplastic exposure triggered oxidative stress, inflammation, and a form of cell death called necroptosis in kidney tissue through the NF-kappaB and RIP1/RIP3/MLKL signaling pathways.
The effect of the cyclic GMP-AMP synthase-stimulator of interferon genes signaling pathway on organ inflammatory injury and fibrosis
This review examined the role of the cGAS-STING innate immune signaling pathway in the pathomechanisms of disease across multiple organs, focusing on its involvement in fibrosis, inflammation, and infection responses. Understanding STING pathway activation has implications for therapeutic targeting in conditions linked to environmental stressors including nanoplastic-induced inflammation.
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.
Polystyrene microplastic-induced extracellular vesicles cause kidney-related effects in the crosstalk between tubular cells and fibroblasts
Researchers found that polystyrene microplastics cause kidney tubule cells to release tiny signaling packages (extracellular vesicles) that trigger stress responses and scarring in neighboring kidney cells. This cell-to-cell communication pathway spread the damage beyond the cells directly exposed to the microplastics. The findings suggest a mechanism by which microplastic exposure could contribute to kidney fibrosis and long-term kidney damage in humans.
Polystyrene nanoplastics reprogramed pulmonary metabolisms mediated by immune regulation of myeloid hypoxia-inducible factor 1α
Researchers exposed mice to polystyrene nanoplastics through their lungs for six weeks and found the particles triggered lung inflammation, scarring, and a metabolic switch to glycolysis — the same energy-burning pattern seen in activated immune cells during injury. A key protein called HIF-1α in immune cells was identified as the driver of these metabolic changes, offering a potential target for understanding nanoplastic lung toxicity.
Protective Effects of Cysteine-Rich Peptides against Microplastics-Induced Cardiorenal Injury via Nrf2/HO-1 and Bax/Cytc Pathways
Researchers found that microplastic exposure caused significant heart and kidney injury in mice, as shown by elevated biomarkers of organ damage. Treatment with cysteine-rich peptides reduced these injury markers by more than 30%, working through activation of protective antioxidant pathways and suppression of cell-death signaling. The study suggests that certain bioactive peptides may help counteract organ damage associated with microplastic exposure.
#5502 Pro-inflammatory Effects of Bisphenol a and Polyethylene Microplastics on Human Renal Tubular Cells
Laboratory experiments showed that both bisphenol A (BPA) and polyethylene microplastics activate inflammatory pathways in human kidney tubular cells, and their combination amplifies this effect through the so-called "Trojan Horse" mechanism. Exposure triggered the aryl hydrocarbon receptor and elevated pro-inflammatory cytokines linked to kidney fibrosis. These findings suggest that combined exposure to microplastics and chemical additives may contribute to the rising global burden of chronic kidney disease.
Exosome‐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.
PVC Nanoplastics Exposure Exacerbates Asthma through R‐Loop Accumulation and Subsequent STING Activation in Macrophages
Researchers investigated how PVC nanoplastics influence asthma using a mouse model and found that the particles worsened airway inflammation. The nanoplastics activated a specific immune signaling pathway in lung macrophages by causing DNA-RNA hybrid structures to accumulate in cells. The study suggests that inhaled nanoplastics may aggravate respiratory conditions through previously unrecognized molecular mechanisms.