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September 21, 2025Burns & TraumaOpen Access

Histone Lactylation Exacerbates Acute Lung Injury in Septic Mice by Promoting Ferroptosis in Pulmonary Microvascular Endothelial Cells

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Authors

PFPu FangSLShuai LiZLZong-Qing Lu

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Overview

This study reveals how lactate influences ferroptosis in pulmonary endothelial cells during sepsis, exacerbating microvascular dysfunction.

Key Points

  • Elevated lactate levels during sepsis increase ferroptosis in pulmonary microvascular endothelial cells, worsening acute lung injury.
  • Histone lactylation was identified as a key factor promoting lipid peroxidation and ferroptosis in pulmonary microvascular dysfunction.
  • The study utilized a septic mouse model, with primary endothelial cell experiments, transcriptomic sequencing, and validation through in vivo and in vitro methods.
  • High serum lactate levels correlated with increased ferroptosis and poor prognosis in patients with sepsis-associated acute respiratory distress syndrome.

Cite This Study

Fang et al. (2025) studied this question.

synapsesocial.com/papers/68d43afa713b0b5dfea7ab05https://doi.org/10.1093/burnst/tkaf056
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Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1Ferroptosis in sepsis induced acute lung injury/acute respiratory distress syndrome (ALI/ARDS): a potential therapeutic strategy2025
  2. 2<scp>METTL14</scp> Inhibits Human Lung Microvascular Endothelial Cell From Ferroptosis in Septic Lung Injury by Regulating <scp> N <sup>6</sup> </scp> ‐Methyladenosine‐Modified <scp>ACSL4</scp> Level2025
  3. 3Lactate metabolic reprogramming and histone lactylation modification in sepsis2025
  4. 4Global Lactylome Reveals Lactylation‐Dependent Mechanisms Underlying CXC Motif Chemokine Ligand 12 Expression in Pulmonary Endothelium During Acute Respiratory Distress Syndrome2025 · 3 citations
  5. 5Elevated lactate production exacerbates PM2.5-induced pulmonary fibrosis by stabilizing TGF-β12025