Description
The calcineurin inhibitor immunosuppressant cyclosporin A (CsA) soon gained clinical application, and became a standard of care in organ transplantation, as well as an important treatment option in a variety of autoimmune diseases. The immunosuppressive effect of CsA is mainly attributed to inhibiting calcineurin phosphatase activity, consequently favouring the inactive phosphorylated form of nuclear factor of activated T cells (NFAT). Renal toxicity is a serious adverse effect of CsA, but the underlying mechanisms are insufficiently understood.; CsA has also been shown to induce episodic hypoxia (Fhling et al, 2017; doi: 10.1111/apha.12811). Here, we sought to identify molecular mechanisms of CsA nephrotoxicity.
Overall Design
Renal injury is observed following 6 weeks of daily CsA treatment. To identify pathways leading to CsA nephrotoxicity, mice were subjected to one week of daily CsA treatment. Kidneys were harvested and global gene expression profiles were analyzed.
Curator
hy_li