Molecular mechanisms contributing to the pathogenesis of severe COVID-19 in pregnant women. mdpi.com/1999-4915/13/1…
mdpi.com/1282034 #mdpiviruses vía @VirusesMDPI @MDPIOpenAccess @INPer_mx
mdpi.com/1282034 #mdpiviruses vía @VirusesMDPI @MDPIOpenAccess @INPer_mx
Spike protein of SARS-CoV-2 virus binds to trophoblastic cells expressing ACE-2, (1) blocking the conversion of ANG-II into ANG 1-7.
(2) Accumulation of ANG-II on the cell surface enhances its binding to the AT-1 receptor (AT-1R), promoting downstream signaling, followed by rapid endocytosis of the ANG-II/AT-1R complex.
(3) By avoiding the endosome/lysosome degradation, the excess of ANG-II is accumulated in endothelial cells. (4) ANG-II binds to mitochondrial AT-1R, inducing cellular senescence with positive regulation of reactive.
(5) Over-activation of AT-1R on the cell membrane leads to increased PKC and calcineurin activity. (6) Transcription factors NF-kB and NFAT are activated and translocated to the nucleus, leading to an increase in gene expression and release of Flt-1.
(7) Flt-1 alternative splicing generates sFlt-1 isoform. (8) The excess of sFlt-1 protein is released into the circulation causing endothelial dysfunction.
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