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61,005 resultsShowing papers similar to Research progress on damage-associated molecular patterns in acute kidney injury
ClearToxicological 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.
Acute kidney injury: exploring endoplasmic reticulum stress-mediated cell death
This review examines how endoplasmic reticulum stress, a cellular response to accumulated misfolded proteins, can trigger various forms of cell death in acute kidney injury. While not directly about microplastics, these same stress pathways are activated when cells are exposed to nanoplastics, which have been shown to accumulate in kidney tissue. Understanding these mechanisms helps explain how microplastic exposure could contribute to kidney damage at the cellular level.
Effects of microplastics on the kidneys: a narrative review
This review summarizes growing evidence that microplastics can accumulate in the kidneys, where they may trigger inflammation, oxidative stress, and cellular damage that could worsen kidney function. People with chronic kidney disease may be especially vulnerable because impaired kidney filtration could allow microplastics to build up more readily in their bodies.
Microplastics and CKD: Are we overlooking the role of ecotoxins
This review argues that microplastics deserve greater consideration as a contributing factor to chronic kidney disease, synthesizing evidence that MPs can accumulate in renal tissue, trigger inflammation and oxidative stress, and may represent an underappreciated environmental driver of CKD.
Microparticles as Potential Mediators of High Glucose-Induced Renal Cell Injury.
This study investigates the role of microparticles — small vesicles shed by cells — in kidney disease progression under high-glucose conditions, testing their involvement in cellular stress pathways relevant to diabetic nephropathy. The paper uses 'microparticles' to refer to cell-derived vesicles rather than environmental plastic particles, and is not related to plastic pollution.
The microplastics exposure induce the kidney injury in mice revealed by RNA-seq
In a mouse study, microplastics of different sizes caused kidney injury including inflammation, oxidative stress, and scarring (fibrosis) after long-term exposure. The smallest particles (80 nanometers) altered immune-related genes, while larger particles disrupted genes tied to the body's internal clock. This research provides evidence that microplastics accumulating in the body over time could contribute to kidney disease in mammals, including humans.
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.
Micro/nano plastics in the urinary system: Pathways, mechanisms, and health risks.
This review synthesizes emerging evidence on how micro- and nano-plastics reach the urinary system, accumulate in kidney and bladder tissue, and cause damage through oxidative stress, inflammation, and disruption of cellular function. The authors conclude that the urinary system is a primary site of microplastic accumulation and call for more research on long-term health impacts.
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.
Environmental toxicants and nephrotoxicity: Implications on mechanisms and therapeutic strategies
This review examines how environmental toxicants, including microplastics, phthalates, and bisphenol A, can damage the kidneys. These substances can accumulate in kidney tissue after being swallowed, inhaled, or absorbed through the skin, triggering inflammation, oxidative stress, and cell death. The findings highlight that the kidneys, which filter about 200 liters of fluid daily, are particularly vulnerable to harm from the growing levels of plastic-related pollutants in our environment.
Polystyrene microplastics induce nephrotoxicity through DDIT4-mediated autophagy and apoptosis
Using lab-grown human kidney tissue, researchers showed that polystyrene microplastics damaged kidney development by triggering a specific stress protein called DDIT4 that led to cell self-destruction. The microplastics impaired the formation of kidney tubules, the structures that filter blood and produce urine. When the researchers blocked DDIT4, the damage was reduced, identifying a potential target for understanding how microplastic exposure might harm kidney health in humans.
Microplastics and Kidneys: An Update on the Evidence for Deposition of Plastic Microparticles in Human Organs, Tissues and Fluids and Renal Toxicity Concern
This review summarizes the growing evidence that microplastics are found throughout the human body, including in the placenta, lungs, liver, heart, blood, and breast milk. While direct evidence for kidney damage in humans is still lacking, animal studies show that microplastics can cause kidney inflammation, cell death, and oxidative stress. The findings highlight that microplastics are accumulating in virtually every human organ, though the long-term health consequences remain unclear.
The threat of microplastics to human kidney health: Mechanisms of nephrotoxicity and future research directions
This review examines the growing evidence that microplastics can reach and damage human kidneys, where they were first detected in 2023. Short-term exposure triggers oxidative stress and inflammation, while long-term exposure may lead to kidney scarring through a process called ferroptosis, a type of cell death linked to iron buildup. The authors propose that microplastics may also activate the immune system in kidneys through a gut-kidney connection, highlighting that kidney health is an important but overlooked concern in microplastic research.
Toxicological effects and mechanisms of renal injury induced by inhalation exposure to airborne nanoplastics
Researchers studied what happens to mouse kidneys after breathing in airborne polystyrene nanoplastics and found the particles accumulated in kidney tissue after entering through the lungs. The nanoplastics activated stress and inflammation pathways that led to kidney cell damage and death. Testing on lab-grown human kidney organoids showed they were even more sensitive to nanoplastic exposure than standard cell lines, suggesting developing kidneys in embryos could be particularly vulnerable.
Polystyrene microplastics induce kidney injury via gut barrier dysfunction and C5a/C5aR pathway activation
In a mouse study, polystyrene microplastics caused kidney damage by first breaking down the gut barrier, which then triggered an immune response that attacked the kidneys through a specific pathway called C5a/C5aR. When researchers repaired the gut barrier or blocked this immune pathway, the kidney damage was prevented. This study reveals a gut-kidney connection that could explain how swallowing microplastics might lead to kidney problems in humans.
Effects of Microplastic (MP) Exposure at Environmentally Relevant Doses on the Structure, Function, and Transcriptome of the Kidney in Mice
Researchers exposed mice to polystyrene microplastics at doses matching levels found in the environment and examined the effects on kidney structure and function. While the microplastics did not cause obvious physical damage to the kidneys, they altered blood markers of kidney function and changed gene expression patterns related to immune response and metabolism. The study suggests that even low-level microplastic exposure may subtly affect kidney biology at the molecular level.
The detrimental effects of microplastic exposure on kidney function
This review explores the two-way relationship between kidney function and microplastic exposure, asking whether MPs can be cleared renally and whether kidney disease impairs their clearance. Evidence suggests MPs accumulate in kidney tissue and may contribute to disease progression, though clinical data remain limited.
Effects of Orally Ingested Microplastics on the Structure and Function of the Kidneys
This study reviewed the structural and functional effects of orally ingested microplastics on kidney tissue, synthesizing experimental evidence from animal and in vitro studies. Microplastic exposure was consistently associated with kidney histopathology including inflammation and fibrosis, with particle size, shape, and polymer type influencing the severity of renal damage.
Microplastic exposure and its consequences for renal and urinary health: systematic review of in vivo studies
This systematic review examines animal studies on how microplastic exposure affects the kidneys and urinary system. The evidence suggests that microplastics can accumulate in kidney tissue and may cause inflammation and oxidative stress, raising concerns about potential long-term effects on human kidney health as our exposure to these particles continues to grow.
Therapeutic potential of Ganoderma lucidum polysaccharide peptide in Doxorubicin-induced nephropathy: modulation of renin-angiotensin system and proteinuria
This paper is not directly about microplastics — it evaluates a polysaccharide peptide from Ganoderma lucidum mushroom as a treatment for doxorubicin-induced kidney injury in mice, finding it inhibits the renin-angiotensin system and reduces proteinuria.
Effects of nano- and microplastics on kidney: Physicochemical properties, bioaccumulation, oxidative stress and immunoreaction
Researchers exposed mice to polystyrene nano- and microplastics of varying sizes and tracked their accumulation and effects in the kidneys. They found that the particles changed their physical properties during digestion, accumulated in kidney tissue, and caused oxidative stress and immune responses. The study suggests that plastic particle size plays an important role in determining the extent of kidney-related harm.
Microplastics Exacerbate Cadmium-Induced Kidney Injury by Enhancing Oxidative Stress, Autophagy, Apoptosis, and Fibrosis
Researchers exposed mice to microplastics and cadmium for three months and found that microplastics significantly worsened cadmium-induced kidney injury. The combined exposure enhanced oxidative stress, autophagy, cell death, and tissue scarring in the kidneys beyond what cadmium alone caused. The study suggests that microplastics may act as amplifiers of heavy metal toxicity in organ systems.
#6225 Microplastics: First Extended Proteomic Analysis on Kidney Tubular Cells
In a preliminary proteomic study, researchers analyzed protein expression changes in kidney tubular cells exposed to microplastics and nanoplastics, identifying disrupted pathways that shed light on the cellular mechanisms by which plastic particles may cause kidney damage.
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.