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Related Experiment Video

Updated: Aug 23, 2025

Evaluation of a Reliable Biomarker in a Cecal Ligation and Puncture-Induced Mouse Model of Sepsis
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DNA-PKcs promotes sepsis-induced multiple organ failure by triggering mitochondrial dysfunction.

Rongjun Zou1, Jun Tao2, Junxiong Qiu2

  • 1Department of Cardiovascular Surgery, Guangdong Provincial Hospital of Chinese Medicine, the Second Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou 510120, Guangdong, China; The Second Clinical College of Guangzhou University of Chinese Medicine, Guangzhou 510405, Guangdong, China.

Journal of Advanced Research
|November 3, 2022
PubMed
Summary

Targeting DNA-dependent protein kinase catalytic subunit (DNA-PKcs) may prevent organ damage in sepsis. Reducing DNA-PKcs improves mitochondrial function and protects organs like the heart, liver, and kidneys from sepsis-induced injury.

Keywords:
DNA-PKcsHeartMODSMitochondriaSepsis

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Area of Science:

  • Biochemistry
  • Molecular Biology
  • Pathophysiology

Background:

  • Sepsis frequently leads to multiple organ dysfunction syndrome (MODS), a major cause of mortality.
  • Mitochondrial dysfunction is a key factor in the progression of sepsis-related MODS.

Purpose of the Study:

  • To investigate the role of DNA-dependent protein kinase catalytic subunit (DNA-PKcs) in sepsis-induced mitochondrial dysfunction.
  • To elucidate the impact of DNA-PKcs on organ damage during sepsis.

Main Methods:

  • Generated organ-specific DNA-PKcs knockout mouse models (cardiomyocyte, liver, kidney).
  • Induced sepsis using lipopolysaccharide (LPS) and assessed organ damage via echocardiography, serum biochemistry, and microscopy.
  • Analyzed mitochondrial function, dynamics, metabolism, and apoptosis using molecular and cellular assays.

Main Results:

  • DNA-PKcs deletion attenuated myocardial damage by enhancing mitochondrial metabolism.
  • Loss of DNA-PKcs protected the liver from sepsis-induced oxidative damage and apoptosis.
  • DNA-PKcs deficiency preserved kidney function by normalizing mitochondrial dynamics, mitophagy, and biogenesis.

Conclusions:

  • DNA-PKcs plays a critical role in sepsis-induced mitochondrial dysfunction and organ damage.
  • Targeting DNA-PKcs presents a potential therapeutic strategy for mitigating sepsis-related MODS.