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61,005 resultsShowing papers similar to Klotho-mediated activation of the anti-oxidant Nrf2/ARE signal pathway affects cell apoptosis, senescence and mobility in hypoxic human trophoblasts: involvement of Klotho in the pathogenesis of preeclampsia
ClearMicroplastic exposure induces preeclampsia-like symptoms via HIF-1α/TFRC-mediated ferroptosis in placental trophoblast cells
Researchers exposed pregnant rats to polystyrene microplastics and found that the particles induced symptoms resembling preeclampsia, including elevated blood pressure and increased protein in urine. The microplastics triggered a type of cell death called ferroptosis in placental cells by activating a specific signaling pathway that led to iron overload and oxidative damage. The study identifies microplastic-induced placental cell death as a potential mechanism linking environmental plastic exposure to pregnancy complications.
Evaluation of polyethylene microplastics toxicity using Nrf2/ARE and MAPK/Nrf2 signaling pathways
Researchers exposed male and female rats to varying doses of polyethylene microplastics and found dose-dependent increases in oxidative stress markers and disruptions to reproductive hormone levels. They identified specific cellular signaling pathways, including the Nrf2 antioxidant response system, that were affected by microplastic exposure. The study suggests that microplastic ingestion may trigger oxidative damage and reproductive effects through identifiable molecular mechanisms.
Role of the Nrf2 Signaling Pathway in Ovarian Aging: Potential Mechanism and Protective Strategies
This review explores how the Nrf2 signaling pathway, a key defense system against oxidative stress, plays a role in ovarian aging, which leads to menopause, reduced fertility, and health risks like osteoporosis. While not focused on microplastics specifically, the Nrf2 pathway is one of the main systems that microplastics disrupt when they accumulate in reproductive tissues. Understanding this pathway helps explain how environmental pollutants like microplastics could accelerate ovarian aging and harm fertility.
Nrf2-dependent redox regulation protects myoblasts from polystyrene nanoplastic-induced premature senescence
Researchers showed that polystyrene nanoplastics trigger premature senescence (accelerated aging) in mouse muscle precursor cells by downregulating the antioxidant regulator Nrf2, and that activating Nrf2 with sulforaphane — a compound found in broccoli — significantly protected cells by restoring mitochondrial integrity and reducing oxidative stress markers.
Gestational exposure to nanoplastics disrupts fetal development by promoting the placental aging via ferroptosis of syncytiotrophoblast
This mouse study found that exposure to nanoplastics during pregnancy caused placental aging and fetal growth restriction through a process called ferroptosis -- a type of iron-dependent cell death -- in the cells that form the barrier between mother and baby. When researchers blocked the ferroptosis process, fetal weight improved, suggesting this pathway could be a target for protecting pregnancies from nanoplastic-related harm.
Redox regulation in aging muscles: exercise as a key modulator to combat sarcopenia and frailty
Researchers reviewed evidence on how aerobic and resistance exercise modulates redox homeostasis in aging skeletal muscle, synthesizing findings from randomized controlled trials and meta-analyses to show that exercise reduces oxidative stress markers by 10–20%, enhances antioxidant enzyme activity by 15–30%, and improves muscle strength and frailty scores through pathways including Nrf2, AMPK, and PGC-1α activation.
Morroniside Protects Human Granulosa Cells against H2O2-Induced Oxidative Damage by Regulating the Nrf2 and MAPK Signaling Pathways
Researchers found that morroniside protects human ovarian granulosa cells from oxidative damage by activating the Nrf2 antioxidant pathway and reducing apoptosis through regulation of p38 and JNK signaling pathways.
High Prolactin Concentration Induces Ovarian Granulosa Cell Oxidative Stress, Leading to Apoptosis Mediated by L-PRLR and S-PRLR
This paper is not relevant to microplastics research — it investigates how high prolactin concentrations induce oxidative stress and apoptosis in ovine ovarian granulosa cells, a reproductive endocrinology study.
Enhanced toxic effects of photoaged microplastics on the trophoblast cells
Researchers investigated how light-aged polystyrene microplastics affect placental function in pregnant mice and found that aged particles caused greater harm than pristine ones. Oral exposure to microplastics starting early in pregnancy impaired fetal growth and damaged the placental tissue layer. The enhanced toxicity of aged microplastics appears to be linked to changes in their physical properties and increased lipid peroxidation in trophoblast cells.
2,7-Phloroglucinol-6,6′-bieckol from Ecklonia cava ameliorates nanoplastics-induced premature endothelial senescence and dysfunction
Researchers found that a compound called PHB derived from the marine algae Ecklonia cava protects coronary artery cells from nanoplastic-induced premature aging and vascular dysfunction by reducing oxidative stress, suppressing senescence-promoting proteins, and restoring nitric oxide production essential for blood vessel relaxation.
Bisphenol-A disrupts mitochondrial functionality leading to senescence and apoptosis in human amniotic mesenchymal stromal cells
Researchers studied how bisphenol-A, a chemical released during microplastic degradation, affects stem cells from the human placental membrane that normally protects the developing fetus. They found that BPA exposure damaged mitochondrial function, increased harmful reactive oxygen species, and triggered premature cell aging and death in these protective cells. The findings raise concerns about how microplastic-derived chemicals encountered during pregnancy could potentially compromise the placental barrier.
Omaveloxolone Prevents Polystyrene Microplastic-Induced Ovarian Granulosa Cell Apoptosis via the Keap1/Nrf2/HO-1 Pathway in Rats
Researchers exposed female rats to polystyrene microplastics for 90 days and found significant oxidative damage and cell death in ovarian tissue. They discovered that the drug omaveloxolone could protect against this damage by activating a cellular defense pathway called Keap1/Nrf2/HO-1. The study suggests that microplastic exposure may pose risks to reproductive health, but also identifies a potential protective mechanism worth further investigation.
The Antioxidative Action of ZTP by Increasing Nrf2/ARE Signal Pathway
This study investigated the antioxidant properties of a compound called ZTP and its ability to protect against oxidative stress in brain tissue. While focused on neuroprotection rather than microplastics, oxidative stress is one of the primary mechanisms by which microplastics are thought to cause cellular damage.
SGLT2 inhibition ameliorates nano plastics-induced premature endothelial senescence and dysfunction
Researchers found that nanoplastics cause premature aging and dysfunction in blood vessel lining cells, and that an SGLT2 inhibitor drug could help counteract these effects. The nanoplastics triggered oxidative stress and inflammation in endothelial cells, which are linked to cardiovascular problems. The study suggests a potential therapeutic approach to address some of the vascular damage associated with nanoplastic exposure.
Oxidative stress-activated Nrf2 remitted polystyrene nanoplastic-induced mitochondrial damage and inflammatory response in HepG2 cells
Researchers discovered that polystyrene nanoplastics damage human liver cells by causing oxidative stress and mitochondrial damage, but the cells activate a protective pathway called Nrf2 to fight back. When the Nrf2 defense was blocked, the damage from nanoplastics became significantly worse, confirming its protective role. This study helps explain how the liver tries to defend itself against nanoplastic toxicity, and suggests that people with weaker antioxidant defenses may be more vulnerable to liver damage from plastic exposure.
Resveratrol Attenuates Oxidative Stress-Induced Intestinal Barrier Injury through PI3K/Akt-Mediated Nrf2 Signaling Pathway
This study investigated the antioxidant compound resveratrol as a potential treatment for oxidative stress-induced intestinal barrier damage, finding it protected gut lining integrity through a specific cell signaling pathway. While focused on intestinal health generally, the mechanisms studied are relevant to how microplastic exposure can damage gut barriers.
Microplastics caused embryonic growth retardation and placental dysfunction in pregnant mice by activating GRP78/IRE1α/JNK axis induced apoptosis and endoplasmic reticulum stress
When pregnant mice were fed polystyrene microplastics, their embryos showed growth delays and their placentas were damaged through a specific stress pathway involving the endoplasmic reticulum, the cell's protein-processing center. These findings suggest that microplastic exposure during pregnancy could interfere with fetal development by triggering cell death in placental tissue.
Placental Micro- and Nanoplastic Contamination: A Systematic Review of Eco-Exposome Pathways to Preterm Birth and Neonatal Outcomes
This systematic review examined evidence that micro- and nanoplastics have been found in human placentas and may be linked to preterm birth. The particles appear to cause inflammation, oxidative stress, and disruption of placental function through multiple molecular pathways, raising concerns about the impact of plastic pollution on pregnancy outcomes and newborn health.
Adverse effects of a realistic concentration of human exposure to microplastics on markers of placental barrier permeability in pregnant rats
Researchers exposed pregnant rats to polystyrene microplastics at concentrations realistic for human exposure and examined effects on the placenta. They found that the microplastics accumulated in placental tissue, caused oxidative stress, triggered cell death, and reduced the expression of proteins that maintain the placental barrier. The study provides the first evidence that realistic levels of microplastic exposure can compromise the protective barrier between mother and developing offspring.
Polystyrene nanoplastics induce ovarian granulosa cell senescence via autophagy suppression
Researchers found that polystyrene nanoplastics induce premature cellular aging (senescence) in human ovarian granulosa cells by suppressing autophagy, triggering inflammatory signaling and mitochondrial dysfunction, and that restoring autophagy with rapamycin reversed these effects — pointing to a potential mechanism linking nanoplastic exposure to accelerated ovarian aging.
Co-exposure to polystyrene microplastics and lead aggravated ovarian toxicity in female mice via the PERK/eIF2α signaling pathway
Researchers found that combined exposure to polystyrene microplastics and lead caused more severe ovarian damage in female mice than either pollutant alone. The study showed that co-exposure activated endoplasmic reticulum stress through the PERK/eIF2-alpha signaling pathway, leading to increased cell death in ovarian tissue, but these effects could be alleviated with stress inhibitor or antioxidant treatment.
ox-LDL-Induced Endothelial Progenitor Cell Oxidative Stress via p38/Keap1/Nrf2 Pathway
Researchers investigated the molecular pathway by which oxidized low-density lipoprotein induces oxidative stress in endothelial progenitor cells, identifying the p38/Keap1/Nrf2 signaling cascade as the key mechanism. They found that ox-LDL activation of this pathway resulted in endothelial progenitor cell dysfunction and apoptosis, implicating this pathway in cardiovascular disease progression.
Morroniside protect human granulosa cells against H2O2-induced oxidative damage via regulating Nrf2 and MAPK signaling pathway
This study investigated whether morroniside, a compound from the Cornus plant, can protect ovarian cells from oxidative stress-induced damage. The research found protective effects in lab experiments, relevant to understanding how environmental oxidative stressors—including pollutants like microplastics—may affect female reproductive cells.
OX-LDL promotes insufficient autophagy and apoptosis of ovarian granulosa cells through regulation ROS-mediated PI3K/Akt/mTOR pathway
This study investigated how oxidized low-density lipoprotein (OX-LDL) triggers cell death in ovarian granulosa cells through oxidative stress pathways. The research identified specific molecular signaling cascades involved in follicle cell damage. While not directly about microplastics, oxidative stress pathways of the type studied here are also activated by microplastic exposure, making this relevant to understanding plastic-related reproductive health risks.