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Identification and Quantification of Deranged Metabolites in Critically Ill Patients Using NMR-Based Metabolomics
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Time-Resolved Metabolomics Reveals Mitochondrial Protection in Septic Liver Injury.

Naoki Suzuki1, Shoichiro Shibata1, Masahiro Sugimoto2,3

  • 1Department of Anesthesiology, Tokyo Medical University, Tokyo 1600023, Japan.

Metabolites
|September 26, 2025
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Summary
This summary is machine-generated.

Cyclophilin D knockout mice show improved resistance to sepsis-induced liver injury by preserving mitochondrial function and reducing oxidative stress. Targeting mitochondrial permeability transition may offer a novel therapeutic strategy for sepsis.

Keywords:
cyclophilin Dliver injurymetabolomicsmitochondrial dysfunctionmitochondrial permeability transitionmousesepsis

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Area of Science:

  • Biochemistry
  • Pathophysiology
  • Mitochondrial Biology

Background:

  • Sepsis is a life-threatening organ dysfunction caused by infection.
  • Mitochondrial dysfunction is implicated in sepsis pathogenesis, but mechanisms are unclear.

Purpose of the Study:

  • Investigate the role of cyclophilin D (CypD) in sepsis-induced liver injury.
  • Elucidate molecular mechanisms of mitochondrial dysfunction in sepsis.

Main Methods:

  • Cecal ligation and puncture (CLP) model of sepsis in wild-type and CypD knockout mice.
  • Liquid chromatography-tandem mass spectrometry (LC-MS/MS) for metabolomic profiling of liver tissues.
  • Analysis of key metabolites, oxidative stress markers, and mitochondrial function indicators.

Main Results:

  • CypD knockout mice maintained stable lactate levels and preserved AMP compared to wild-type mice.
  • Increased glutathione disulfide (GSSG) and spermidine, with decreased malondialdehyde (MDA) in CypD knockout mice, indicating reduced oxidative stress.
  • CypD deficiency mitigated liver injury and preserved mitochondrial function during sepsis.

Conclusions:

  • CypD deficiency protects against sepsis-induced liver injury.
  • Targeting mitochondrial permeability transition pore (mPTP) offers a potential therapeutic avenue for sepsis.
  • Mitochondrial function and oxidative stress are critical in sepsis pathogenesis.