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Renal Cyclosporin-A (CsA) toxicity

ABSTRACT: 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 (Fähling et al, 2017; doi: 10.1111/apha.12811). Here, we sought to identify molecular mechanisms of CsA nephrotoxicity.

ORGANISM(S): Mus musculus

PROVIDER: GSE111516 | GEO | 2021/02/22

REPOSITORIES: GEO

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Renal Cyclosporin-A (CsA) toxicity

Project description:Renal Cyclosporin-A (CsA) toxicity

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Comparative Transcriptional and Phenotypic Peripheral Blood Analysis of Kidney Recipients under Cyclosporin A or Sirolimus Monotherapy

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Cyclosporin A inhibits prostate cancer growth through suppression of E2F8

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Cyclosporin ameliorates right ventricular remodeling of postnatal mice with volume overload.

Project description:We reported the RNAseq analyses of right ventricular free wall of myocardium in three groups of mice（3 in each group）at postnatal day 14 (P14). The mice in volume overload (VO) group underwent an abdominal surgery by puncture from aorta to inferior vena cava at P7, mice in Sham group underwent the same surgery except for the puncture. The mice in CsA group were VO mice who were also injected with cyclosporin A(CsA) for seven days. The results revealed that there were differentially expressed genes between VO and sham group at P14, Inhibiting the immune response with CsA caused the gene expression profile of VO mice to shift towards that of sham mice.

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Project description:The incidence of new onset diabetes after transplant (NODAT) has increased over the past decade, likely due to calcineurin inhibitor-based immunosuppressants, including tacrolimus (TAC) and cyclosporin (CsA). Voclosporin (VCS), a next generation calcineurin inhibitor is reported to cause fewer incidences of NODAT but the reason is unclear. Whilst calcineurin signaling plays important roles in pancreatic beta-cell survival, proliferation, and function, its effects on human beta-cells remain understudied. In particular, we do not understand why some calcineurin inhibitors have more profound effects on the incidence of NODAT. Here, we compared the the effects of TAC and VCS on the transcriptomic profile of human islets.

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