Researchers found that a stress-signaling protein called ATF4 drives kidney cell death and inflammation after drug exposure, and that blocking it with a new compound or gene-silencing nanoparticles significantly protected kidney function in mice.
1
ATF4 was markedly upregulated in damaged kidney tubule cells in both human and mouse AKI models, and its deletion significantly reduced kidney dysfunction and inflammation.
2
ATF4 drives pyroptosis (inflammatory cell death) by activating the STAT1-GBP2 signaling axis, which then triggers NLRP3 inflammasome assembly.
3
Two therapeutic strategies, the ISR antagonist ERMT1 and engineered nanobiologics silencing ATF4 in tubule cells, both significantly reduced renal injury in preclinical models.
mail
Weekly plant science — one email, Saturdays.
Check your inbox to confirm — link expires in 24 hours.
Something went wrong — please try again.
Too many signup attempts from your network. Try again in an hour, or email hello@plant.news.