Use my Search Websuite to scan PubMed, PMCentral, Journal Hosts and Journal Archives, FullText.
Kick-your-searchterm to multiple Engines kick-your-query now !>
A dictionary by aggregated review articles of nephrology, medicine and the life sciences
Your one-stop-run pathway from word to the immediate pdf of peer-reviewed on-topic knowledge.

suck abstract from ncbi


10.1038/s41418-021-00866-0

http://scihub22266oqcxt.onion/10.1038/s41418-021-00866-0
suck pdf from google scholar
34518653!8435761!34518653
unlimited free pdf from europmc34518653    free
PDF from PMC    free
html from PMC    free

suck abstract from ncbi


Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534

Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534
pmid34518653      Cell+Death+Differ 2022 ; 29 (2): 420-438
Nephropedia Template TP

gab.com Text

Twit Text FOAVip

Twit Text #

English Wikipedia


  • Fatal cytokine release syndrome by an aberrant FLIP/STAT3 axis #MMPMID34518653
  • Musiu C; Caligola S; Fiore A; Lamolinara A; Frusteri C; Del Pizzo FD; De Sanctis F; Cane S; Adamo A; Hofer F; Barouni RM; Grilli A; Zilio S; Serafini P; Tacconelli E; Donadello K; Gottin L; Polati E; Girelli D; Polidoro I; Iezzi PA; Angelucci D; Capece A; Chen Y; Shi ZL; Murray PJ; Chilosi M; Amit I; Bicciato S; Iezzi M; Bronte V; Ugel S
  • Cell Death Differ 2022[Feb]; 29 (2): 420-438 PMID34518653show ga
  • Inflammatory responses rapidly detect pathogen invasion and mount a regulated reaction. However, dysregulated anti-pathogen immune responses can provoke life-threatening inflammatory pathologies collectively known as cytokine release syndrome (CRS), exemplified by key clinical phenotypes unearthed during the SARS-CoV-2 pandemic. The underlying pathophysiology of CRS remains elusive. We found that FLIP, a protein that controls caspase-8 death pathways, was highly expressed in myeloid cells of COVID-19 lungs. FLIP controlled CRS by fueling a STAT3-dependent inflammatory program. Indeed, constitutive expression of a viral FLIP homolog in myeloid cells triggered a STAT3-linked, progressive, and fatal inflammatory syndrome in mice, characterized by elevated cytokine output, lymphopenia, lung injury, and multiple organ dysfunctions that mimicked human CRS. As STAT3-targeting approaches relieved inflammation, immune disorders, and organ failures in these mice, targeted intervention towards this pathway could suppress the lethal CRS inflammatory state.
  • |Aged[MESH]
  • |Aged, 80 and over[MESH]
  • |Animals[MESH]
  • |COVID-19/metabolism/*physiopathology[MESH]
  • |Caspase 8/metabolism[MESH]
  • |Cytokine Release Syndrome/*etiology/*metabolism[MESH]
  • |Cytokines/immunology/metabolism[MESH]
  • |Female[MESH]
  • |Humans[MESH]
  • |Inflammation/*metabolism[MESH]
  • |Male[MESH]
  • |Mice[MESH]
  • |Mice, Inbred C57BL[MESH]
  • |Middle Aged[MESH]
  • |SARS-CoV-2/immunology[MESH]
  • |STAT3 Transcription Factor/genetics/*metabolism[MESH]


  • DeepDyve
  • Pubget Overpricing
  • suck abstract from ncbi

    Linkout box