文献引用
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1) Targeting of Tumoral NAC1 Mitigates Myeloid-Derived Suppressor Cell-Mediated Immunosuppression and Potentiates Anti-PD-1 Therapy in Ovarian Cancer.
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2) MAPK4 inhibits the early aberrant activation of B cells in rheumatoid arthritis by promoting the IRF4-SHIP1 signaling pathway.
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3) Dysregulation of sphingolipid metabolism contributes to the pathogenesis of chronic myeloid leukemia.
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4) Trifluridine/tipiracil induces ferroptosis by targeting p53 via the p53-SLC7A11 axis in colorectal cancer 3D organoids.
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5) Chemotherapy-induced macrophage CXCL7 expression drives tumor chemoresistance via the STAT1/PHGDH-serine metabolism axis and SAM paracrine feedback to M2 polarization.
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6) Bone marrow mesenchymal stem cells alleviate neurological dysfunction by reducing autophagy damage via downregulation of SYNPO2 in neonatal hypoxic-ischemic encephalopathy rats.
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7) Deletion of Tfap2a in hepatocytes and macrophages promotes the progression of hepatocellular carcinoma by regulating SREBP1/FASN/ACC pathway and anti-inflammatory effect of IL10.
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8) Ubiquitin-specific protease 7 regulates macrophage polarization via pyruvate kinase M2-mediated metabolic reprogramming in severe acute pancreatitis.
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9) FAM135B Deficiency Inhibits Cytotoxic T-Cell Activity in Triple-negative Breast Cancer by Blocking the IFI16-dependent STING Pathway.
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10) HIF-1α alleviates ferroptosis in ulcerative colitis by regulation of GPX4.
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11) Aβ -induced excessive mitochondrial fission drives type H blood vessels injury to aggravate bone loss in APP/PS1 mice with Alzheimer's diseases.
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12) Physical Exercise Decreases Complement-Mediated Synaptic Loss and Protects Against Cognitive Impairment by Inhibiting Microglial Tmem9-ATP6V0D1 in Alzheimer's Disease.
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13) Synergistic effects of mTOR inhibitors with VEGFR3 inhibitors on the interaction between TSC2-mutated cells and lymphatic endothelial cells.
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14) Vine tea (Ampelopsis grossedentata) ameliorates chronic alcohol-induced hepatic steatosis, oxidative stress, and inflammation via YTHDF2/PGC-1α/SIRT3 axis.
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15) Aβ -induced excessive mitochondrial fission drives type H blood vessels injury to aggravate bone loss in APP/PS1 mice with Alzheimer's diseases.