Monocytes serve as Shiga toxin carriers during the development of hemolytic uremic syndrome.

Shiga toxin (Stx)-induced hemolytic uremic syndrome (HUS) poses a life-threatening complication for which a definitive treatment remains elusive. To exert its cytotoxic effect on renal cells, Stx must be delivered from the infected intestines to the kidney. However, the mechanism underlying Stx delivery remains unclear.

YTHDF1 mitigates acute kidney injury via safeguarding mA-methylated mRNAs in stress granules of renal tubules.

Acute kidney injury (AKI) presents a daunting challenge with limited therapeutic options. To explore the contribution of N-methyladenosine (mA) in AKI development, we have investigated mA-modified mRNAs within renal tubular cells subjected to injuries induced by diverse stressors. Notably, while the overall level of mA-modified RNA remains unaltered in renal tubular cells facing stress, a distinct phenomenon emerges-mRNAs bearing mA methylation exhibit a pronounced tendency to accumulate within stress granules (SGs), structures induced in response to these challenges.