文献引用
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1) Nicotinamide Mononucleotide (NMN) Improves the Senescence of Mouse Vascular Smooth Muscle Cells Induced by Ang II Through Activating p-AMPK/KLF4 Pathway.
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2) Glutathione-protected Au22 Nanoclusters Ameliorates Hypoxic-Ischemic Brain Damage in Neonatal Rats via Sirt3/SOD2 Signaling Pathway.
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3) S-phase kinase-associated protein 1 inhibits orbital fibroblasts adipogenesis to improve thyroid-associated ophthalmopathy (TAO).
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4) Protective effects of Salidroside against ferroptosis through PPARG-dependent mechanism in diabetes-related cognitive impairment.
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5) Influence of Sevoflurane Postconditioning on Hypoxic-Ischemic Brain Injury via Nrf2-Regulated Ferroptosis in Neonatal Rats.
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6) Cellular effects of splenectomy on liver regeneration after 70% resection.
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7) Suppression of NOX2-Derived Reactive Oxygen Species (ROS) Reduces Epithelial-to-MesEnchymal Transition Through Blocking SiO2-Regulated JNK Activation.
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8) Overexpression of colonic VIP ameliorates cognitive function and barrier system damage caused by sevoflurane anesthesia and surgery in aged rats with fragile brain functions.
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9) ACVR1 drives neuropathic pain by regulating NLRP3-Induced neuronal pyroptosis through the p38 and Smad1/5/8 pathways.
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10) Inhibition of tRF- 02514 in Extracellular Vesicles Preserves Microglia Pyroptosis and Protects Against Parkinson's Disease.
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11) Localized sclerostin accumulation in osteocyte lacunar-canalicular system is associated with cortical bone microstructural alterations and bone fragility in db/db male mice.
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12) Carnosol mitigates Ang II-stimulated vascular injury and oxidative stress by directly binding to FAK and inhibiting its activation.
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13) Exosomal PD-L1 derived from hypoxia nasopharyngeal carcinoma cell exacerbates CD8+ T cell suppression by promoting PD-L1 upregulation in macrophages.
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14) Identification and verification of international neuroblastoma staging system (INSS) stage-related genes as potential biomarkers for neuroblastoma prognostic models.
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15) The role of astrocyte-derived extracellular vesicles in cellular microenvironment remodeling after spinal cord injury: A study based on quantitative proteomics analysis.