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61,005 resultsShowing papers similar to Inter- and intracellular mitochondrial communication: signaling hubs in aging and age-related diseases
ClearMicroplastics/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.
Micro- and nanoplastic-induced mitochondrial dysfunction and organelle miscommunication: A toxicological perspective
This review examined how micro- and nanoplastics disrupt mitochondrial function and inter-organelle communication in cells. The evidence indicates that these particles cause oxidative stress, calcium dysregulation, impaired energy production, and activation of stress responses including autophagy and cell death, with cascading effects on lysosomes, the endoplasmic reticulum, and nuclear function.
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.
Author comment: Mitochondria as a target of micro- and nanoplastic toxicity — R0/PR1
This review examines how microplastics and nanoplastics disrupt the function of mitochondria — the cell's energy-producing organelles — by triggering oxidative stress, altering membrane potential, and interfering with cell signaling. Because mitochondrial dysfunction is linked to neurodegenerative disease, cancer, diabetes, and cardiovascular conditions, this work raises concern that microplastic exposure could contribute to or worsen these diseases. The authors call for more targeted research into how plastic particles interact with cellular energy systems.
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.
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.
Author comment: Mitochondria as a target of micro- and nanoplastic toxicity — R1/PR4
This review details how micro- and nanoplastics disrupt mitochondria — the energy-producing structures inside cells — by generating reactive oxygen species, altering membrane potential, and interfering with the quality-control processes cells use to maintain healthy mitochondria. Because mitochondrial dysfunction is a common driver of neurodegenerative diseases, cancer, diabetes, and cardiovascular disease, these findings suggest a plausible cellular mechanism linking plastic particle exposure to serious chronic illness. The review calls for more research into mitochondria as a key target of plastic toxicity.
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.
Role of Mitochondria in Intestinal Epithelial Barrier Dysfunction in Inflammatory Bowel Disease
This review examines the role of mitochondrial dysfunction in the breakdown of the intestinal epithelial barrier in inflammatory bowel disease. Researchers highlight how impaired mitochondrial function in intestinal cells can contribute to increased gut permeability and inflammation, pointing to mitochondria as a potential focus for future therapeutic strategies.
Mitochondrial Quality Control and Metabolic Reprogramming in Hepatocellular Carcinoma: Implications for Immunotherapy and Treatment Resistance
Scientists reviewed research showing that liver cancer cells damage the tiny energy factories (mitochondria) inside immune cells, making it harder for the body's natural defenses to fight the cancer. When immune cells can't get enough energy, they become "exhausted" and stop working properly against tumors. The researchers suggest that targeting these energy problems in cells could help improve cancer treatments and make immunotherapy work better for liver cancer patients.
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.
Role of mitochondria-associated membranes (MAMs) in inflammatory signaling: implications for acute lung injury pathogenesis
This review examines how dysfunction of mitochondria-associated membranes — contact zones between the endoplasmic reticulum and mitochondria — contributes to inflammatory signaling and acute lung injury pathogenesis through dysregulated calcium signaling, lipid metabolism, and inflammatory activation.
Role of Mitochondria in Inflammatory Bowel Diseases: A Systematic Review
This systematic review found that mitochondrial dysfunction plays a significant role in inflammatory bowel diseases through multiple mechanisms, including disrupted energy production, impaired mucosal repair, altered gut microbiota signaling, and weakened intestinal barrier integrity. The findings are relevant to microplastic research because plastic particle exposure has been shown to cause mitochondrial damage in gut tissues.
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.
Nano-sized microplastics exposure induces skin cell senescence via triggering the mitochondrial localization of GSDMD
Researchers found that nano-sized microplastics enter skin cells and trigger premature aging (senescence) by damaging the energy-producing structures inside cells (mitochondria) and activating inflammatory pathways. This study suggests that microplastic exposure could accelerate skin aging and inflammation, adding to concerns about the health effects of plastic pollution on organs exposed to the environment.
Mitochondrial dysfunction–induced PANoptosis: Mechanisms, triggers, and disease implications
This review provides a comprehensive overview of PANoptosis, a recently identified form of cell death that combines features of three previously distinct pathways: pyroptosis, apoptosis, and necroptosis. Researchers describe how mitochondrial dysfunction can trigger this integrated cell death response, with implications for infections, inflammation, cancer, and degenerative diseases. The study highlights PANoptosis as an important emerging concept for understanding how cells respond to environmental and biological stressors.
Bisphenol A Disrupts Mitochondrial Functionality Leading to Senescence and Apoptosis in Human Amniotic Mesenchymal Stromal Cells
This study investigated how bisphenol A disrupts mitochondrial function in cells, finding that BPA exposure induces mitochondrial stress, promotes cellular senescence, and triggers apoptosis at environmentally relevant concentrations.
Recommendation: Mitochondria as a target of micro- and nanoplastic toxicity — R2/PR8
This review examines how micro- and nanoplastics target mitochondria in cells, disrupting energy production, triggering oxidative stress, altering membrane potential and mitochondrial dynamics, and potentially contributing to neurodegenerative, cardiovascular, and metabolic disease development.
Molecular mechanisms underlying mitochondrial damage, endoplasmic reticulum stress, and oxidative stress induced by environmental pollutants
This review examines how environmental pollutants including microplastics, heavy metals, and pesticides damage cells by disrupting mitochondria, triggering endoplasmic reticulum stress, and generating harmful reactive oxygen species. Researchers describe the molecular signaling pathways through which these pollutants cause cell dysfunction and death. The study highlights the interconnected nature of these cellular stress responses and their relevance to understanding pollution-related health effects.
Decision: Mitochondria as a target of micro- and nanoplastic toxicity — R0/PR3
Microplastics and nanoplastics can enter human cells and directly damage mitochondria — the organelles that power every cell — by triggering oxidative stress, disrupting energy production, and activating cell death pathways. Because mitochondrial dysfunction underlies diseases ranging from neurodegeneration to cancer and diabetes, this review argues that mitochondrial harm should be treated as a central mechanism linking plastic exposure to chronic disease risk.
The 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.
Recommendation: Mitochondria as a target of micro- and nanoplastic toxicity — R0/PR2
This review focuses on mitochondria as a key target of micro- and nanoplastic toxicity, summarizing evidence that MPs and NPs trigger oxidative stress, disrupt mitochondrial membrane potential, alter fusion/fission dynamics, and activate mitophagy. Because mitochondrial dysfunction underlies neurodegenerative disease, diabetes, and cancer, this mechanistic framework helps explain why microplastic exposure may contribute to a wide range of serious human health conditions.
Micro- and Nanoplastics Exposure Across the Lifespan: One Health Implications for Aging and Longevity
Researchers reviewed evidence on micro- and nanoplastic exposure across the human lifespan through a One Health lens, finding that MNPs trigger oxidative stress, inflammation, mitochondrial dysfunction, and cellular senescence—mechanisms central to aging—and that older adults face compounded risk from lifetime accumulation and diminished physiological resilience, though direct epidemiological data in this population remain sparse.