Tacrolimus (TAC) is a first-line immunosuppressant used to prevent rejection after solid-organ transplantation, yet its clinical utility is limited by nephrotoxicity, which can progress to irreversible kidney injury or graft loss. The molecular mechanisms underlying TAC-induced nephrotoxicity remain insufficiently understood. Here, we systematically assessed TAC responses across human in vitro nephron model: proximal tubule cells sorted from iPSC-derived kidney organoids.
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