Tacrolimus induces fibroblast-to-myofibroblast transition via a TGF-β-dependent mechanism to contribute to renal fibrosis
Adaku C. Ume, Tara Yesomi Wenegieme, Jennae N. Shelby, Chiagozie D. B. Paul-Onyia, Aston M. J. Waite, John Karanja Kamau, Danielle N. Adams, Keiichiro Susuki, Eric S. Bennett, Hongmei Ren, Clintoria R. Williams
Abstract
Renal fibrosis, a detrimental feature of irreversible kidney damage, remains a sinister consequence of long-term calcineurin inhibitor (CNI) immunosuppressive therapy. Our study not only incorporates renal fibroblasts into the growing list of cell types negatively impacted by CNIs but also identifies renal fibroblast-to-myofibroblast transition as a process mediated via a TGF-β-dependent mechanism. This insight will direct future studies investigating the feasibility of inhibiting TGF-β signaling to maintain CNI-mediated immunosuppression while ultimately preserving kidney health.