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10.3390/v13122383 http://scihub22266oqcxt.onion/10.3390/v13122383 34960652!8708337!34960652     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=34960652&cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\34960652.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Viruses 2021 ; 13 (12): � Nephropedia Template TP {{tp|p=34960652|t=2021. Inhibiting ACSL1-Related Ferroptosis Restrains Murine Coronavirus Infection |pdf=|usr=}}{{34960652}} gab.com Text Inhibiting ACSL1-Related Ferroptosis Restrains Murine Coronavirus Infection JO: Viruses http://www.kidney.de/pget.php?&tw=1&pmid=34960652 #FOAvip Murine hepatitis virus strain A59 (MHV-A59) was shown to induce pyroptosis, apoptosis, and necroptosis of infected cells, especially in the murine macrophages. However, whether ferroptosis, a recently identified form of lytic cell death, was involved in the pathogenicity of MHV-A59 is unknown. We utilized murine macrophages and a C57BL/6 mice intranasal infection model to address this. In primary macrophages, the ferroptosis inhibitor inhibited viral propagation, inflammatory cytokines released, and cell syncytia formed after MHV-A59 infection. In the mouse model, we found that in vivo administration of liproxstatin-1 ameliorated lung inflammation and tissue injuries caused by MHV-A59 infection. To find how MHV-A59 infection influenced the expression of ferroptosis-related genes, we performed RNA-seq in primary macrophages and found that MHV-A59 infection upregulates the expression of the acyl-CoA synthetase long-chain family member 1 (ACSL1), a novel ferroptosis inducer. Using ferroptosis inhibitors and a TLR4 inhibitor, we showed that MHV-A59 resulted in the NF-kB-dependent, TLR4-independent ACSL1 upregulation. Accordingly, ACSL1 inhibitor Triacsin C suppressed MHV-A59-infection-induced syncytia formation and viral propagation in primary macrophages. Collectively, our study indicates that ferroptosis inhibition protects hosts from MHV-A59 infection. Targeting ferroptosis may serve as a potential treatment approach for dealing with hyper-inflammation induced by coronavirus infection. Twit Text FOAVip Inhibiting ACSL1-Related Ferroptosis Restrains Murine Coronavirus Infection ????Viruses http://www.kidney.de/pget.php?&tw=1&pmid=34960652 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=34960652 #FOAvip English Wikipedia <ref>{{Cite pmid|34960652}}</ref> Inhibiting ACSL1-Related Ferroptosis Restrains Murine Coronavirus Infection #MMPMID34960652 Xia H; Zhang Z; You F Viruses 2021[Nov]; 13 (12): � PMID34960652show ga Murine hepatitis virus strain A59 (MHV-A59) was shown to induce pyroptosis, apoptosis, and necroptosis of infected cells, especially in the murine macrophages. However, whether ferroptosis, a recently identified form of lytic cell death, was involved in the pathogenicity of MHV-A59 is unknown. We utilized murine macrophages and a C57BL/6 mice intranasal infection model to address this. In primary macrophages, the ferroptosis inhibitor inhibited viral propagation, inflammatory cytokines released, and cell syncytia formed after MHV-A59 infection. In the mouse model, we found that in vivo administration of liproxstatin-1 ameliorated lung inflammation and tissue injuries caused by MHV-A59 infection. To find how MHV-A59 infection influenced the expression of ferroptosis-related genes, we performed RNA-seq in primary macrophages and found that MHV-A59 infection upregulates the expression of the acyl-CoA synthetase long-chain family member 1 (ACSL1), a novel ferroptosis inducer. Using ferroptosis inhibitors and a TLR4 inhibitor, we showed that MHV-A59 resulted in the NF-kB-dependent, TLR4-independent ACSL1 upregulation. Accordingly, ACSL1 inhibitor Triacsin C suppressed MHV-A59-infection-induced syncytia formation and viral propagation in primary macrophages. Collectively, our study indicates that ferroptosis inhibition protects hosts from MHV-A59 infection. Targeting ferroptosis may serve as a potential treatment approach for dealing with hyper-inflammation induced by coronavirus infection. |*Ferroptosis[MESH] |Animals[MESH] |Coenzyme A Ligases/*antagonists & inhibitors/genetics/*metabolism[MESH] |Coronavirus Infections/*therapy[MESH] |Cytokines/metabolism[MESH] |Disease Models, Animal[MESH] |Genes, Viral[MESH] |Lung Injury/pathology[MESH] |Macrophages[MESH] |Mice[MESH] |Mice, Inbred C57BL[MESH] |Murine hepatitis virus[MESH] |Quinoxalines[MESH] |RAW 264.7 Cells[MESH] |Spiro Compounds[MESH] |Toll-Like Receptor 4[MESH]Inhibiting ACSL1-Related Ferroptosis Restrains Murine Coronavirus Infe(epmc).pdf DeepDyve Pubget Overpricing