{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Ellsworth CR"],"funding":["American Heart Association","American Heart Association-American Stroke Association","NHLBI NIH HHS","NIH","U.S. Department of Veterans Affairs","NIH HHS"],"pagination":["405"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11405604"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["81(1)"],"pubmed_abstract":["Emerging evidence indicates that activation of complement system leading to the formation of the membrane attack complex (MAC) plays a detrimental role in COVID-19. However, their pathogenic roles have never been experimentally investigated before. We used three knock out mice strains (1. C3<sup>-/-</sup>; 2. C7<sup>-/-</sup>; and 3. Cd59ab<sup>-/-</sup>) to evaluate the role of complement in severe COVID-19 pathogenesis. C3 deficient mice lack a key common component of all three complement activation pathways and are unable to generate C3 and C5 convertases. C7 deficient mice lack a complement protein needed for MAC formation. Cd59ab deficient mice lack an important inhibitor of MAC formation. We also used anti-C5 antibody to block and evaluate the therapeutic potential of inhibiting MAC "],"journal":["Cellular and molecular life sciences : CMLS"],"pubmed_title":["Enhanced complement activation and MAC formation accelerates severe COVID-19."],"pmcid":["PMC11405604"],"funding_grant_id":["R01 HL165265","P51 OD011104","R01HL165265","HL139930","AHA962950","R01DK129881","IK6BX005235","962950","P51OD011104-62"],"pubmed_authors":["Qian C","Khatun MS","Wang C","Maness NJ","Islamuddin M","Halperin JA","Qin X","Liu S","Kolls JK","Xiao MT","Blair RV","Chen Z","Tomlinson S","Ellsworth CR"],"additional_accession":[]},"is_claimable":false,"name":"Enhanced complement activation and MAC formation accelerates severe COVID-19.","description":"Emerging evidence indicates that activation of complement system leading to the formation of the membrane attack complex (MAC) plays a detrimental role in COVID-19. However, their pathogenic roles have never been experimentally investigated before. We used three knock out mice strains (1. C3<sup>-/-</sup>; 2. C7<sup>-/-</sup>; and 3. Cd59ab<sup>-/-</sup>) to evaluate the role of complement in severe COVID-19 pathogenesis. C3 deficient mice lack a key common component of all three complement activation pathways and are unable to generate C3 and C5 convertases. C7 deficient mice lack a complement protein needed for MAC formation. Cd59ab deficient mice lack an important inhibitor of MAC formation. We also used anti-C5 antibody to block and evaluate the therapeutic potential of inhibiting MAC ","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Sep","modification":"2026-06-02T23:16:51.024Z","creation":"2025-04-04T12:09:25.372Z"},"accession":"S-EPMC11405604","cross_references":{"pubmed":["39284944"],"doi":["10.1007/s00018-024-05430-w"]}}