Showing 1,541 - 1,560 results of 8,229 for search '"inflammation"', query time: 0.08s Refine Results
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    Foodborne toxin Aflatoxin B1 induced glomerular podocyte inflammation through proteolysis of RelA, downregulation of miR-9 and CXCR4/TXNIP/NLRP3 pathway by Jie Zhang, Shuang Yang, Baocai Xu, Zihui Qin, Xinyi Guo, Ben Wei, Qinghua Wu, Kamil Kuca, Tushuai Li, Wenda Wu

    Published 2024-07-01
    “…AFB1 induces podocyte inflammation, proteinuria and renal dysfunction. Studying the mechanism of AFB1-induced podocyte inflammation and murine kidney dysfunction, we detected that AFB1 increased ubiquitin-dependent degradation of the transcription factor RelA through enhanced interaction of RelA with E3 ubiquitin ligase tripartite motif containing 7 (TRIM7) in mouse podocyte clone-5 (MPC-5) and mouse glomeruli. …”
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    Small Extracellular Vesicles Secreted by iPSC-Derived MSCs Ameliorate Pulmonary Inflammation and Lung Injury Induced by Sepsis through Delivery of miR-125b-5p by Wei Peng, Yun Yang, Jiaquan Chen, Zeyao Xu, Yuanlei Lou, Qi Li, Ning Zhao, Kejian Qian, Fen Liu

    Published 2023-01-01
    “…Results. iMSC-sEV were able to attenuate pulmonary inflammation and lung injury following CLP-induced lung injury. iMSC-sEV were internalized by AMs and alleviated the release of inflammatory factors by inactivating the NF-κB signaling pathway. …”
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    New Paradigm in Cell Therapy Using Sperm Head to Restore Brain Function and Structure in Animal Model of Alzheimer’s Disease: Support for Boosting Constructive Inflammation vs. Anti-Inflammatory Approach by Nafiseh Pakravan, Ardeshir Abbasi, Zuhair Mohammad Hassan

    Published 2022-01-01
    “…Alzheimer’s is characterized by accumulation of amyloid-β (Aβ) associated with insufficient clearance of toxicants from the brain establishing a chronic inflammation and other abnormalities in the brain. Inflammatory microglia and astrocytes along with abnormal lymphatics associated with insufficient clearance of Aβ and other toxicants from the brain establish a chronic inflammation. …”
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