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61,005 resultsShowing papers similar to Microplastics induce insulin resistance by causing mitochondrial dysfunction associated with mROS in skeletal muscle in vitro
ClearThe impact of oxidative stress-induced mitochondrial dysfunction on diabetic microvascular complications
This review examines how high blood sugar in diabetes triggers excessive production of reactive oxygen species (ROS) in mitochondria, leading to a destructive cycle of cellular damage that drives complications in the heart, kidneys, and blood vessels. While focused on diabetes, this mechanism is relevant to microplastic research because microplastics are also known to increase ROS production and mitochondrial dysfunction in human cells.
The Impact of Micro-Nanoplastics on Mitochondria in the Context of Diet and Diet-Related Diseases
This review examines how micro- and nanoplastics may worsen diet-related diseases like obesity and type 2 diabetes by damaging mitochondria, the energy-producing structures inside cells. Studies suggest that microplastic exposure combined with unhealthy diets can amplify metabolic problems like insulin resistance and high blood sugar. The findings point to mitochondrial damage as a key link between microplastic exposure and the growing epidemic of metabolic diseases.
Polystyrene microplastics-induced ROS overproduction disrupts the skeletal muscle regeneration by converting myoblasts into adipocytes
Researchers found that polystyrene microplastics impaired skeletal muscle repair in mice by triggering excess production of reactive oxygen species (ROS) inside muscle stem cells. This oxidative stress redirected muscle stem cells to become fat cells instead of new muscle fibers, resulting in increased fat deposits and reduced muscle fiber size. The study suggests that microplastic exposure could interfere with the body's natural ability to regenerate and maintain muscle tissue.
Exposure to polystyrene nanoplastics promotes premature cellular senescence through mitochondrial ROS production and dysfunction in pre-differentiated skeletal myoblasts
This lab study found that polystyrene nanoplastics caused premature aging in muscle precursor cells by damaging their mitochondria and triggering excessive production of harmful molecules called reactive oxygen species. The nanoplastics were absorbed into cells, accumulated there, and caused the cells to stop dividing and show signs of aging. This suggests that nanoplastic exposure could contribute to muscle deterioration and aging-related conditions by damaging the cells responsible for muscle repair.
Impact of Micro- and Nanoplastics on Mitochondria
This review examines how micro- and nanoplastics can damage mitochondria, the energy-producing structures inside cells that are critical for metabolism and cell survival. Researchers found that plastic particle exposure can trigger oxidative stress, disrupt mitochondrial membrane function, and interfere with energy production pathways. Since mitochondrial dysfunction is linked to numerous health conditions, the study suggests this may be a key mechanism through which plastic pollution affects human health.
Polystyrene microplastics (PS-MPs) disturb skeleto-muscular energy metabolism and tissue architecture following sub-acute exposure: A dose-responsive study
Wistar rats given polystyrene microplastics in drinking water (0.5–50 mg/L) for 28 days showed dose-dependent disruption of skeletal muscle energy metabolism — including reduced ATP production and altered mitochondrial activity — along with histological changes in muscle tissue architecture.
Mitochondria as a target of micro- and nanoplastic toxicity
This review examines how micro- and nanoplastics damage mitochondria, the energy-producing structures inside our cells. Research shows these tiny plastic particles can cross biological barriers, enter cells, and disrupt mitochondrial function by triggering oxidative stress and altering energy production. Since mitochondrial damage is linked to diseases like cancer, diabetes, and neurodegeneration, this represents a key concern for human health.
Micro- and nanoplastic impact on insulin resistance and related metabolic disorder in rodents: A systematic review
This systematic review examined whether micro- and nanoplastics contribute to insulin resistance in animal studies. The findings suggest that polystyrene plastic particles can disrupt how the body processes sugar and responds to insulin, pointing to a possible link between plastic exposure and metabolic disorders like type 2 diabetes.
Dissection of the potential mechanism of polystyrene microplastic exposure on cardiomyocytes
Researchers investigated how polystyrene microplastics affect human heart muscle cells at concentrations reflecting estimated daily human intake levels. They found that the microplastics caused oxidative stress, mitochondrial dysfunction, and disrupted calcium signaling in the cells. The study suggests that microplastic exposure may contribute to cardiovascular risks by directly damaging heart cell function at the cellular level.
Polystyrene nanoplastics promote muscle cell senescence through microtubule hyper-stabilization-mediated mitophagy dysfunction and cGAS-Sting activation
Researchers found that polystyrene nanoplastics cause premature aging in human muscle cells by disrupting the internal skeleton of cells and impairing the cleanup of damaged mitochondria. The nanoplastics made the cell's structural framework too rigid, which blocked normal cell signaling and triggered an inflammatory aging response. This study suggests that nanoplastic exposure could contribute to muscle weakness and age-related muscle loss in humans.
Polystyrene microplastic exposure induces insulin resistance in mice via dysbacteriosis and pro-inflammation
Researchers found that exposing mice to polystyrene microplastics induced insulin resistance regardless of whether the animals were on a normal or high-fat diet. The study identified disruption of gut bacteria and increased intestinal inflammation as key mechanisms driving the metabolic changes. These findings suggest that microplastic exposure may contribute to metabolic health issues by altering the gut microbiome and triggering chronic inflammation.
Adverse Effect of Polystyrene Nanoplastics in Impairing Glucose Metabolism in Liver Injury
Polystyrene nanoplastics disrupted glucose metabolism in liver cells by interfering with insulin signaling pathways and mitochondrial function, suggesting that nanoplastic exposure could contribute to metabolic disorders including insulin resistance.
Amino-Functionalized Polystyrene Nano-Plastics Induce Mitochondria Damage in Human Umbilical Vein Endothelial Cells
Researchers found that amino-functionalized polystyrene nanoplastics can damage mitochondria in human umbilical vein endothelial cells, which line blood vessels. The study suggests that nanoplastics small enough to enter the body through the food chain may pose risks to the cardiovascular system by disrupting cellular energy production and triggering oxidative stress in vascular cells.
The Mitochondrial Battleground: A Review of Microplastic-Induced Oxidative Stress and Inflammatory Pathways in Human Health
This review synthesizes research on how microplastics damage mitochondria through oxidative stress and inflammation across aquatic, terrestrial, and mammalian systems. Researchers found that microplastics generate reactive oxygen species that disrupt mitochondrial function, with smaller and aged particles causing greater toxicity, while inflammatory signaling creates a feedback loop that worsens cellular damage.
Influence of Polystyrene Microplastics on Mitochondrial Oxidative Damage in Renal and Muscular Tissues of the Freshwater Fish
Researchers exposed freshwater fish to environmentally relevant concentrations of polystyrene microplastics for up to 15 days and examined mitochondrial damage in kidney and muscle tissues. The exposure disrupted antioxidant defenses, increased oxidative stress, and altered metabolic enzyme activities in both tissue types. Histological examination revealed significant tissue damage including necrosis and degeneration, suggesting that microplastics can cause organ-level toxicity in fish through mitochondrial oxidative stress.
Testicular mitochondrial redox imbalance and impaired oxidative phosphorylation underlie microplastic-induced testicular dysfunction in Wistar rats
Researchers investigated how polyethylene microplastics affect male reproductive function in rats by examining testicular mitochondrial health. The study found that microplastic exposure disrupted mitochondrial redox balance and impaired oxidative phosphorylation in testicular tissue, providing mechanistic evidence for how microplastics may contribute to male reproductive toxicity.
Polystyrene microplastics impair the functions of cultured mouse Leydig (TM3) and Sertoli (TM4) cells by inducing mitochondrial-endoplasmic reticulum damage
Lab experiments showed that polystyrene microplastics damaged two key types of testicular cells in mice -- Leydig cells that produce testosterone and Sertoli cells that support sperm development -- by harming their mitochondria (the cell's energy centers) and stressing the endoplasmic reticulum. These findings suggest that microplastic exposure could contribute to male reproductive problems by disrupting hormone production and sperm development at the cellular level.
Microplastics/nanoplastics contribute to aging and age-related diseases: Mitochondrial dysfunction as a crucial role
This review examines how microplastics and nanoplastics may contribute to aging and age-related conditions by damaging mitochondria, the energy-producing structures inside cells. Researchers describe how these tiny plastic particles enter the body through food, water, and air, and accumulate in various organs where they can disrupt normal mitochondrial function. The study suggests that microplastic-driven mitochondrial damage could be an underappreciated factor in the aging process and related health decline.
Environmental nanoplastics induce mitochondrial dysfunction: A review of cellular mechanisms and associated diseases
This review summarizes how nanoplastics, which are small enough to enter individual cells, damage mitochondria (the energy-producing structures inside cells) by disrupting their shape, function, and ability to produce energy. This mitochondrial damage has been linked to a range of diseases including neurodegeneration, diabetes, cardiovascular disease, and reproductive problems. The findings help explain why nanoplastic exposure may contribute to multiple chronic health conditions through a common cellular mechanism.
Environmental Insults to Glucose Metabolism: The Role of Pollutants in Insulin Resistance
This review examines how environmental pollutants, including microplastics, contribute to insulin resistance, a condition where the body's cells respond poorly to insulin. Researchers summarize evidence linking pollutant exposure to disruptions in glucose and lipid metabolism through mechanisms like oxidative stress and inflammation. The study suggests that environmental contamination may be an underrecognized factor in the growing prevalence of metabolic conditions such as type 2 diabetes.
Assessing micro and nanoplastics toxicity using rodent models: Investigating potential mitochondrial implications
This review examines recent rodent studies investigating how micro- and nanoplastics affect cellular health, with a focus on potential mitochondrial impacts. Researchers found that while no study has directly targeted mitochondrial effects, several reported molecular and biochemical changes consistent with disrupted mitochondrial function, including oxidative stress. The study suggests that mitochondria may be an important but understudied target of micro- and nanoplastic toxicity.
Polystyrene microplastics disrupt adrenal steroid synthesis in male mice via mitochondrial dysfunction
Researchers found that polystyrene microplastics disrupted steroid hormone production in the adrenal glands of male mice by causing mitochondrial dysfunction and oxidative stress. Chronic exposure led to reduced corticosterone levels and increased cell death in adrenal tissue. The study suggests that microplastics may interfere with the body's stress response and hormonal balance through damage to the energy-producing structures within cells.
Mitochondria as a target of micro- and nanoplastic toxicity
This review examines how micro- and nanoplastics damage mitochondria, the energy-producing structures inside cells. Studies show that plastic particles can disrupt energy production, cause harmful oxidative stress, and interfere with the cell's ability to repair or recycle damaged mitochondria. Since mitochondrial damage is linked to many chronic diseases including heart disease, neurodegeneration, and diabetes, this helps explain why microplastic exposure may have widespread health effects.
Polystyrene nanoplastics trigger mitochondrial and metabolic reprogramming in cardiomyocytes: Evidence from integrated transcriptomic and metabolomic analysis
Scientists found that tiny plastic particles called nanoplastics can damage heart cells by disrupting their powerhouses (mitochondria) and reducing their ability to produce energy. When researchers exposed human heart cells and mice to these nanoplastics, they observed weakened heart function and signs of early heart damage. This research suggests that the growing amount of microscopic plastic pollution in our environment could pose previously unknown risks to heart health.