Key result
Histone lactylation drives neodymium oxide-induced pulmonary fibrosis via macrophage-fibroblast crosstalk and PI3K/Akt/mTOR signaling.
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May offer epigenetic targets for lung fibrosis; leaves open clinical translation from preclinical models.
-induced macrophage-fibroblast interactions and elucidate the molecular mechanism underlying the regulation of PIK3R2 expression by H4K12 lactylation. This regulation, in turn, activates the PI3K/Akt/mTOR-signaling pathway and the fibrotic process, thus providing novel potential epigenetic targets for the prevention and treatment of lung fibrosis.
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Li et al. (2026) studied this question. Histone lactylation at H4K12 drives neodymium oxide-induced pulmonary fibrosis by promoting macrophage-fibroblast crosstalk and activating the PIK3R2/PI3K/Akt/mTOR signaling pathway.
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