← brief for 2026-09-06 · Slowing decline

HDAC4 drives ferroptosis and fibrosis by inhibiting Foxo3a-GPX4 axis during AKI–CKD progression

Key takeaways

A protein called HDAC4 pushed kidney cells toward a form of cell death driven by iron, and toward scarring of kidney tissue. It did this by shutting down a protective pathway (Foxo3a and GPX4). The team followed this during the shift from sudden kidney injury to long-term kidney disease. This was done in animals and cells, not in people, so it points to a possible drug target and nothing more.

Who did this work

Fengchen Shen (Shanghai East Hospital) · Xinyu Du (Shanghai East Hospital) · Xinyu Du (Shanghai East Hospital) · Liyuan Yao (Shanghai East Hospital) · Chao Yu (Shanghai East Hospital) · Yanjin Wang (Shanghai East Hospital) · Jianjun Yu (Shanghai East Hospital) · Zhipeng Yan (Shanghai East Hospital) · Yuzhen Zhang (Shanghai East Hospital) · Shougang Zhuang (Shanghai East Hospital) · Shougang Zhuang (Shanghai East Hospital)

Source

Paper · OpenAlex, Kidney disease concept sweep (verified C2778653478) · 2026-09-05
https://doi.org/10.1038/s41419-026-08905-9