Lactylation‑mediated ferroptosis: A novel mechanism and therapeutic prospects in human diseases (Review).

Lysine lactylation (Kla), an emerging post‑translational modification, bidirectionally regulates cell fate decisions through epigenetic reprogramming and the direct modification of key ferroptosis proteins. It drives disease progression or mediates therapeutic resistance in inflammation, neurodegenerative diseases, cancer and ischemia‑reperfusion injury, with its regulatory direction being disease‑type‑dependent. The present review discusses the functions of the Kla‑ferroptosis regulatory network, unraveling the role of Kla‑ferroptosis in diseases and its therapeutic implications. The present review aimed to provide novel perspectives for the treatment of human diseases.