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10.12688/f1000research.25979.2 http://scihub22266oqcxt.onion/10.12688/f1000research.25979.2 33082935!7536583!33082935     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=33082935&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       F1000Res 2020 ; 9 (?): 1078 Nephropedia Template TP {{tp|p=33082935|t=2020. Immunopathology of galectin-3: an increasingly promising target in COVID-19 |pdf=|usr=}}{{33082935}} gab.com Text Immunopathology of galectin-3: an increasingly promising target in COVID-19 JO: F1000Res http://www.kidney.de/pget.php?&tw=1&pmid=33082935 #FOAvip The pandemic brought on by the outbreak of severe acute respiratory syndrome coronavirus 2 (SARS-CoV2) has become a global health crisis, with over 22 million confirmed cases and 777,000 fatalities due to coronavirus disease 2019 (COVID-19) reported worldwide. The major cause of fatality in infected patients, now referred to as the "Cytokine Storm Syndrome" (CSS), is a direct result of aberrant immune activation following SARS-CoV2 infection and results in excess release of inflammatory cytokines, such as interleukin (IL)-1, tumor necrosis factor alpha (TNF-alpha), and IL-6, by macrophages, monocytes, and dendritic cells. Single cell analysis has also shown significantly elevated levels of galectin 3 (Gal-3) in macrophages, monocytes, and dendritic cells in patients with severe COVID-19 as compared to mild disease. Inhibition of Gal-3 reduces the release of IL-1, IL-6, and TNF-alpha from macrophages in vitro, and as such may hold promise in reducing the incidence of CSS. In addition, Gal-3 inhibition shows promise in reducing transforming growth factor ss (TGF-ss) mediated pulmonary fibrosis, likely to be a major consequence in survivors of severe COVID-19. Finally, a key domain in the spike protein of SARS-CoV2 has been shown to bind N-acetylneuraminic acid (Neu5Ac), a process that may be essential to cell entry by the virus. This Neu5Ac-binding domain shares striking morphological, sequence, and functional similarities with human Gal-3. Here we provide an updated review of the literature linking Gal-3 to COVID-19 pathogenesis. Dually targeting galectins and the Neu5Ac-binding domain of SARS-CoV2 shows tentative promise in several stages of the disease: preventing viral entry, modulating the host immune response, and reducing the post-infectious incidence of pulmonary fibrosis. Twit Text FOAVip Immunopathology of galectin-3: an increasingly promising target in COVID-19 ????F1000Res http://www.kidney.de/pget.php?&tw=1&pmid=33082935 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=33082935 #FOAvip English Wikipedia <ref>{{Cite pmid|33082935}}</ref> Immunopathology of galectin-3: an increasingly promising target in COVID-19 #MMPMID33082935 Caniglia JL; Asuthkar S; Tsung AJ; Guda MR; Velpula KK F1000Res 2020[]; 9 (?): 1078 PMID33082935show ga The pandemic brought on by the outbreak of severe acute respiratory syndrome coronavirus 2 (SARS-CoV2) has become a global health crisis, with over 22 million confirmed cases and 777,000 fatalities due to coronavirus disease 2019 (COVID-19) reported worldwide. The major cause of fatality in infected patients, now referred to as the "Cytokine Storm Syndrome" (CSS), is a direct result of aberrant immune activation following SARS-CoV2 infection and results in excess release of inflammatory cytokines, such as interleukin (IL)-1, tumor necrosis factor alpha (TNF-alpha), and IL-6, by macrophages, monocytes, and dendritic cells. Single cell analysis has also shown significantly elevated levels of galectin 3 (Gal-3) in macrophages, monocytes, and dendritic cells in patients with severe COVID-19 as compared to mild disease. Inhibition of Gal-3 reduces the release of IL-1, IL-6, and TNF-alpha from macrophages in vitro, and as such may hold promise in reducing the incidence of CSS. In addition, Gal-3 inhibition shows promise in reducing transforming growth factor ss (TGF-ss) mediated pulmonary fibrosis, likely to be a major consequence in survivors of severe COVID-19. Finally, a key domain in the spike protein of SARS-CoV2 has been shown to bind N-acetylneuraminic acid (Neu5Ac), a process that may be essential to cell entry by the virus. This Neu5Ac-binding domain shares striking morphological, sequence, and functional similarities with human Gal-3. Here we provide an updated review of the literature linking Gal-3 to COVID-19 pathogenesis. Dually targeting galectins and the Neu5Ac-binding domain of SARS-CoV2 shows tentative promise in several stages of the disease: preventing viral entry, modulating the host immune response, and reducing the post-infectious incidence of pulmonary fibrosis. |*Coronavirus Infections/pathology[MESH] |*Cytokine Release Syndrome/virology[MESH] |*Galectin 3/immunology[MESH] |*Pneumonia, Viral/pathology[MESH] |Betacoronavirus[MESH] |COVID-19[MESH] |Humans[MESH] |N-Acetylneuraminic Acid[MESH] |Pandemics[MESH]Immunopathology of galectin-3: an increasingly promising target in COV(epmc).pdf DeepDyve Pubget Overpricing