METTL1 aggravates sepsis-acute kidney injury by promoting m7G methylation of NLRP3-mediated pyroptosis.

. Furthermore, METTL1 knockdown inhibited m7G methylation of NLRP3, thereby reducing its stability. Overexpression of NLRP3 abrogated the inhibition of pyroptosis caused by METTL1 knockdown. In conclusion, silencing of METTL1 alleviates sepsis-induced AKI by inhibiting m7G methylated NLRP3-mediated pyroptosis in renal tubular epithelial cells. These findings suggest that targeting METTL1 may represent a promising therapeutic strategy for managing sepsis-associated AKI.