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10.1016/j.clim.2021.108795

http://scihub22266oqcxt.onion/10.1016/j.clim.2021.108795
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34252574!8270746!34252574
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suck abstract from ncbi


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pmid34252574      Clin+Immunol 2021 ; 229 (ä): 108795
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  • Complement activation and increased expression of Syk, mucin-1 and CaMK4 in kidneys of patients with COVID-19 #MMPMID34252574
  • Jamaly S; Tsokos MG; Bhargava R; Brook OR; Hecht JL; Abdi R; Moulton VR; Satyam A; Tsokos GC
  • Clin Immunol 2021[Aug]; 229 (ä): 108795 PMID34252574show ga
  • Acute and chronic kidney failure is common in hospitalized patients with COVID-19, yet the mechanism of injury and predisposing factors remain poorly understood. We investigated the role of complement activation by determining the levels of deposited complement components (C1q, C3, FH, C5b-9) and immunoglobulin along with the expression levels of the injury-associated molecules spleen tyrosine kinase (Syk), mucin-1 (MUC1) and calcium/calmodulin-dependent protein kinase IV (CaMK4) in the kidney tissues of people who succumbed to COVID-19. We report increased deposition of C1q, C3, C5b-9, total immunoglobulin, and high expression levels of Syk, MUC1 and CaMK4 in the kidneys of COVID-19 patients. Our study provides strong rationale for the expansion of trials involving the use of inhibitors of these molecules, in particular C1q, C3, Syk, MUC1 and CaMK4 to treat patients with COVID-19.
  • |*SARS-CoV-2[MESH]
  • |Aged[MESH]
  • |Aged, 80 and over[MESH]
  • |COVID-19/*metabolism/pathology[MESH]
  • |Calcium-Calmodulin-Dependent Protein Kinase Type 4/genetics/metabolism[MESH]
  • |Complement System Proteins/genetics/*metabolism[MESH]
  • |Fatal Outcome[MESH]
  • |Female[MESH]
  • |Gene Expression Regulation[MESH]
  • |Humans[MESH]
  • |Kidney/*metabolism[MESH]
  • |Male[MESH]
  • |Middle Aged[MESH]
  • |Mucin-1/genetics/*metabolism[MESH]


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