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 Microplastics accumulated in breast cancer patients lead to mitophagy via ANXA2-mediated endocytosis and IL-17 signaling pathway
ClearImpact of Environmental Microplastic Exposure on Caco-2 Cells: Unraveling Proliferation, Apoptosis, and Autophagy Activation
Researchers exposed human intestinal cells to polyethylene and PET microplastics of different sizes and observed significant decreases in cell survival along with increased oxidative stress. The microplastics triggered both programmed cell death (apoptosis) and the cell's self-recycling process (autophagy), with effects varying by particle size. The study suggests that microplastic exposure may compromise the intestinal barrier through multiple pathways of cellular damage.
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.
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.
Microplastics and Nanoplastics in Cancer Progression: Biology and Public Health
This review examines emerging evidence that microplastics and nanoplastics may contribute to cancer-related processes by crossing biological barriers and accumulating in tissues. The study highlights that these particles can cause oxidative stress, inflammation, DNA damage, and barrier dysfunction at the cellular level, and may promote tumor-supporting processes including angiogenesis and immune evasion.
Effects of micro- and nanoplastic exposure on macrophages: a review of molecular and cellular mechanisms
This review details how macrophages, key immune cells, respond when they engulf micro- and nanoplastics. The particles trigger inflammatory signaling, damage mitochondria and lysosomes, cause excessive production of harmful reactive oxygen species, and can lead to cell death, while in fat tissue they promote fat buildup and insulin resistance.
Effects of microplastics on chemo-resistance and tumorigenesis of colorectal cancer
For the first time, researchers confirmed the presence of microplastics in human colorectal cancer tissue and showed in animal models that microplastics increased cancer rates and made tumors more resistant to chemotherapy drugs. The study found that microplastics trigger a cell survival mechanism called autophagy that helps cancer cells resist treatment, suggesting plastic pollution could complicate cancer outcomes.
Insight into the mitochondrial unfolded protein response and cancer: opportunities and challenges
This review explores the mitochondrial unfolded protein response, a cellular stress response that maintains protein quality in mitochondria, and its role in cancer progression. Researchers describe how cancer cells hijack this protective mechanism to repair mitochondria and promote tumor growth and invasion. While not directly about microplastics, the paper provides context for understanding cellular stress responses that may be relevant to how cells respond to environmental contaminants.
An updated systematic review about various effects of microplastics on cancer: A pharmacological and in-silico based analysis
This systematic review with in-silico analysis found that microplastics have both tumor-promoting and tumor-suppressing effects on cancer cells, affecting viability, migration, metastasis, and apoptosis. The study identified key proteins (AP2M1, ASGR2, BI-1, Ferritin Heavy Chain) involved in microplastic-mediated cancer progression and used computational modeling to identify existing drugs that might counteract these pathways.
Microscopic menace: exploring the link between microplastics and cancer pathogenesis
This review examines the growing evidence linking microplastic exposure to cancer development in humans. Microplastics can accumulate in the body and trigger inflammation, oxidative stress, and other biological changes associated with tumor growth. While more clinical research is needed, the review highlights that microplastics should be taken seriously as a potential factor in cancer risk.
Cancer Metabolism: The Role of ROS in DNA Damage and Induction of Apoptosis in Cancer Cells
This review explores how reactive oxygen species (ROS) -- harmful molecules produced during abnormal cell metabolism -- can damage DNA and trigger cancer cell death, making ROS a potential target for cancer treatment. While not directly about microplastics, this is relevant because microplastic exposure is known to increase ROS production in human cells, which could contribute to DNA damage over time.
Microplastic induces mitochondrial pathway mediated cellular apoptosis in mussel (Mytilus galloprovincialis) via inhibition of the AKT and ERK signaling pathway
Researchers exposed mussels to two common types of polystyrene microplastics and found that both triggered programmed cell death in the animals' tissues by disrupting key survival signaling pathways and causing mitochondrial damage. Irregularly shaped microplastics proved more harmful than smooth spherical ones. The study provides evidence that microplastic pollution can cause significant cellular damage in shellfish through specific biological mechanisms.
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.
Microplastic accumulation in endometrial cancer tissues and its metabolic impact
Researchers examined microplastic levels in endometrial cancer tissues compared to normal tissue and found that cancer tissues contained significantly higher concentrations of plastic particles. The most common plastics detected were polyethylene, polypropylene, and polystyrene. Metabolic analysis revealed that microplastic presence was associated with changes in cancer-related metabolic pathways, suggesting that microplastics may play a role in promoting tumor development through metabolic reprogramming.
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 microplastics induce hepatic lipid metabolism and energy disorder by upregulating the NR4A1-AMPK signaling pathway
Researchers found that polystyrene microplastics accumulate in the liver and disrupt fat and energy metabolism by activating a specific molecular pathway called NR4A1-AMPK. This activation triggers a self-cleaning process called autophagy that reduces fat production in liver cells, while also increasing harmful reactive oxygen species. The findings suggest that long-term microplastic exposure could lead to ongoing liver damage through this metabolic disruption.
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.
The influence of microplastic particles on the effectiveness of electrochemotherapy in breast cancer cells
Researchers examined whether microplastic particle exposure affects the effectiveness of electrochemotherapy in breast cancer cells, investigating whether MPs could alter cellular responses to the combined electroporation and chemotherapy treatment through inflammatory or oxidative stress mechanisms.
Polystyrene microplastics exacerbate mitophagy through mitochondrial dysfunction in the duck lung
Ducks fed polystyrene microplastics developed lung inflammation and damage through a process where the plastics disrupted the energy-producing mitochondria in lung cells, triggering excessive cell self-destruction. The study confirmed these findings in both live ducks and lab-grown lung cells, showing that the microplastics activated inflammatory pathways and disrupted normal energy metabolism. Since ducks are widely consumed as food, the research highlights how microplastics can damage poultry lung health and provides insights into how inhaled or ingested microplastics might similarly harm human lungs.
Recent insights into uptake, toxicity, and molecular targets of microplastics and nanoplastics relevant to human health impacts
This review summarizes what scientists know about how tiny plastic particles enter the human body and cause harm at the cellular level, including through inflammation, oxidative stress, and disruption of important cell signaling pathways. Americans are estimated to consume tens of thousands to millions of micro- and nanoplastic particles per year, and these particles can penetrate cells and tissues throughout the body.
Polypropylene microplastics promote metastatic features in human breast cancer
Researchers found that polypropylene microplastics, one of the most common types found in human tissue, promoted the spread and invasion of human breast cancer cells in laboratory experiments. The microplastics activated specific signaling pathways that help cancer cells migrate to other parts of the body. While this is a lab study and not proof that microplastics cause cancer in people, it raises important questions about how chronic microplastic exposure might influence cancer progression.
Microplastics exacerbate ferroptosis via mitochondrial reactive oxygen species-mediated autophagy in chronic obstructive pulmonary disease
Researchers found that microplastics worsen chronic obstructive pulmonary disease (COPD) by triggering a chain reaction in lung cells: the plastics damage mitochondria (the cell's energy centers), which produces harmful molecules that activate a self-destructive process called autophagy-dependent ferroptosis. Lung tissue from COPD patients contained significantly higher concentrations of polystyrene microplastics than healthy controls. When scientists blocked this destructive pathway in mice, it reduced the excessive inflammation and prevented COPD flare-ups caused by microplastic exposure.
In-silico pharmacological insights into the therapeutic potential of microRNAs for microplastic-associated cancers
Researchers systematically screened published literature to identify cancer-related genes altered by microplastic exposure, then computationally evaluated microRNAs with anticancer activity that could target those genes, finding potential miRNA-based therapeutic candidates across breast, gastric, and other microplastic-associated tumor types.
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.
Microplastics aggravates rheumatoid arthritis by affecting the proliferation/migration/inflammation of fibroblast-like synovial cells by regulating mitochondrial homeostasis
Researchers investigated how microplastics affect the joint tissue cells involved in rheumatoid arthritis using lab and animal models. They found that microplastic exposure promoted the growth, spread, and inflammatory activity of these cells, while also worsening cartilage damage through disruption of mitochondrial function. The study suggests that microplastic exposure may aggravate inflammatory joint conditions by interfering with cellular energy processes.