Tacrolimus induces fibroblast-to-myofibroblast transition via a TGF-β-dependent mechanism to contribute to renal fibrosis
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.
Document Details
- Document Type
- Pub Defense Publication
- Publication Date
- May 01, 2023
- Source ID
- 10.1152/ajprenal.00226.2022
Entities
People
- Adaku C Ume
- Aston M. J. Waite 3rd
- Chiagozie D. B. Paul-onyia
- Clintoria R Williams
- Danielle N. Adams
- Eric S. Bennett
- Hongmei Ren
- Jennae N. Shelby
- John K. Kamau
- Keiichiro Susuki
- Tara‐Yesomi Wenegieme
Organizations
- American Heart Association
- American Physiological Society
- American Society of Nephrology
- National Institute of Arthritis and Musculoskeletal and Skin Diseases
- National Institute of Diabetes and Digestive and Kidney Diseases
- National Institute of Neurological Disorders and Stroke
- United States Department of Defense
- Wright State University