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Circadian Gene Expression Rhythms During Critical Illness.

Matthew B Maas1,2,3,4,5,6,7,8, Marta Iwanaszko4, Bryan D Lizza5

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Critical illness disrupts normal body rhythms, causing core clock genes and transcriptome oscillations to become abnormal. This disruption is linked to encephalopathy severity in patients, suggesting new research avenues.

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Area of Science:

  • Circadian biology
  • Critical care medicine
  • Genomics

Background:

  • Core clock genes regulate essential physiological processes through tissue-specific transcriptome oscillations synchronized by the central circadian rhythm.
  • The central circadian rhythm is known to dampen rapidly during critical illness, but its impact on gene expression oscillations remains unclear.

Purpose of the Study:

  • To investigate the rhythmicity and phase coherence of core clock genes and the broader transcriptome in critically ill patients.
  • To compare gene expression patterns in critically ill patients with those of healthy volunteers.

Main Methods:

  • A cross-sectional study involving 15 critically ill patients (sepsis, intracerebral hemorrhage) and 11 healthy controls.
  • Continuous wrist actigraphy and frequent serum melatonin sampling for 24 hours to profile circadian and rest-activity rhythms.
  • Whole blood RNA sequencing to analyze core clock gene rhythmicity and overall transcriptome phase coherence using the TimeSignature algorithm.

Main Results:

  • Healthy controls exhibited significant circadian rhythmicity in five of six core clock genes, whereas critically ill patients showed none.
  • The TimeSignature algorithm revealed significantly higher transcriptome phase disruption in critically ill patients compared to healthy controls (median absolute error 4.90 vs 1.48 hours).
  • Disrupted transcriptome rhythms in critically ill patients correlated with the severity of encephalopathy as measured by the Glasgow Coma Scale.

Conclusions:

  • Critical illness leads to rapid abnormalities in gene expression rhythms.
  • The observed association between disrupted transcriptome rhythms and encephalopathy highlights a potential pathophysiological link requiring further investigation.