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10.1016/j.vph.2021.106879

http://scihub22266oqcxt.onion/10.1016/j.vph.2021.106879
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34051372!8152239!34051372
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suck abstract from ncbi


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pmid34051372      Vascul+Pharmacol 2021 ; 139 (ä): 106879
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  • Crosstalk of TLR4, vascular NADPH oxidase, and COVID-19 in diabetes: What are the potential implications? #MMPMID34051372
  • de Oliveira AA; Nunes KP
  • Vascul Pharmacol 2021[Aug]; 139 (ä): 106879 PMID34051372show ga
  • Toll-like receptor 4 (TLR4) contributes to the pathophysiology of diabetes. This happens, at least in part, because TLR4 modulates the enzyme NADPH oxidase, a primary source of ROS in vascular structures. Increased oxidative stress disrupts key vascular signaling mechanisms and drives the progression of diabetes, elevating the likelihood of cardiovascular diseases. Recently, it has been shown that patients with diabetes are also at a higher risk of developing severe coronavirus disease 2019 (COVID-19). Given the importance of the interaction between TLR4 and NADPH oxidase to the disrupted diabetic vascular system, we put forward the hypothesis that TLR4-mediated NADPH oxidase-derived ROS might be a critical mechanism to help explain why this disparity appears in diabetic patients, but unfortunately, conclusive experimental evidence still lacks in the literature. Herein, we focus on discussing the pathological implications of this signaling communication in the diabetic vasculature and exploring this crosstalk in the context of diabetes-associated severe COVID-19.
  • |Animals[MESH]
  • |Blood Vessels/*enzymology/physiopathology/virology[MESH]
  • |COVID-19/enzymology/physiopathology/*virology[MESH]
  • |Diabetes Mellitus/*enzymology/physiopathology[MESH]
  • |Diabetic Angiopathies/*enzymology/physiopathology[MESH]
  • |Enzyme Activation[MESH]
  • |Host-Pathogen Interactions[MESH]
  • |Humans[MESH]
  • |NADPH Oxidases/*metabolism[MESH]
  • |Oxidative Stress[MESH]
  • |Prognosis[MESH]
  • |Reactive Oxygen Species/metabolism[MESH]
  • |SARS-CoV-2/*pathogenicity[MESH]
  • |Signal Transduction[MESH]


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