SARS-CoV-2 infection triggers profibrotic macrophage responses and lung fibrosis.
Wendisch D, Dietrich O, Mari T, von Stillfried S, Ibarra IL, Mittermaier M, Mache C, Chua RL, Knoll R, Timm S, Brumhard S, Krammer T, Zauber H, Hiller AL, Pascual-Reguant A, Mothes R, Bülow RD, Schulze J, Leipold AM, Djudjaj S, Erhard F, Geffers R, Pott F, Kazmierski J, Radke J, Pergantis P, Baßler K, Conrad C, Aschenbrenner AC, Sawitzki B, Landthaler M, Wyler E, Horst D; Deutsche COVID-19 OMICS Initiative (DeCOI); Hippenstiel S, Hocke A, Heppner FL, Uhrig A, Garcia C, Machleidt F, Herold S, Elezkurtaj S, Thibeault C, Witzenrath M, Cochain C, Suttorp N, Drosten C, Goffinet C, Kurth F, Schultze JL, Radbruch H, Ochs M, Eils R, Müller-Redetzky H, Hauser AE, Luecken MD, Theis FJ, Conrad C, Wolff T, Boor P, Selbach M, Saliba AE, Sander LE.
Wendisch D, et al. Among authors: drosten c.
Cell. 2021 Dec 22;184(26):6243-6261.e27. doi: 10.1016/j.cell.2021.11.033. Epub 2021 Nov 27.
Cell. 2021.
PMID: 34914922
Free PMC article.
Exposure of human monocytes to SARS-CoV-2, but not influenza A virus or viral RNA analogs, was sufficient to induce a similar profibrotic phenotype in vitro. ...
Exposure of human monocytes to SARS-CoV-2, but not influenza A virus or viral RNA analogs, was sufficient to induce a similar profibr …