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

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International journal of molecular medicine 2026 Vol.57(2)
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Lin Z, Zou Y, Zou S, Wen K

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Lysine lactylation (Kla), an emerging post‑translational modification, bidirectionally regulates cell fate decisions through epigenetic reprogramming and the direct modification of key ferroptosis pro

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BibTeX ↓ RIS ↓
APA Lin Z, Zou Y, et al. (2026). Lactylation‑mediated ferroptosis: A novel mechanism and therapeutic prospects in human diseases (Review).. International journal of molecular medicine, 57(2). https://doi.org/10.3892/ijmm.2025.5713
MLA Lin Z, et al.. "Lactylation‑mediated ferroptosis: A novel mechanism and therapeutic prospects in human diseases (Review).." International journal of molecular medicine, vol. 57, no. 2, 2026.
PMID 41384296
DOI 10.3892/ijmm.2025.5713

Abstract

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.

MeSH Terms

Humans; Ferroptosis; Protein Processing, Post-Translational; Animals; Neoplasms; Neurodegenerative Diseases; Lysine; Reperfusion Injury; Inflammation

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