A study in Sprague-Dawley rats and NRK-52E cells demonstrated that the mir-181c was significantly suppressed in kidney tissue after burn injury and further downregulated during burn sepsis, while its ectopic expression reduced LPS-induced TLR4 protein expression, suppressed KIM-1 mRNA, and inhibited inflammatory and chemokine gene expression, ultimately attenuating burn sepsis-induced acute kidney injury [Yu et al. DOI:10.007/s00068-022-02124-5].