Damage-associated molecular patterns derived from mitochondria may contribute to the hemodialysis-associated

Theodoros Eleftheriadis1, Georgios Pissas, Georgia Antoniadi

  • 1Department of Nephrology, Medical School, University of Thessaly, Neo Ktirio, Mezourlo Hill, 41110, Larissa, Greece, teleftheriadis@yahoo.com.

Abstract

Insights

Mitochondrial damage-associated molecular patterns (DAMPs) like cytochrome c and inflammation marker IL-6 are elevated in hemodialysis (HD) patients. Increased cytochrome c correlates with higher IL-6 levels in HD patients.

Area of Science:

  • Nephrology
  • Immunology
  • Cell Biology

Background:

  • Inflammation is a frequent complication in patients undergoing hemodialysis (HD).
  • Mitochondrial damage-associated molecular patterns (DAMPs) contribute to inflammation, released during cell death.
  • Increased cellular apoptosis in HD patients suggests elevated DAMPs release.

Purpose of the Study:

  • To evaluate serum levels of cytochrome c, a marker of mitochondrial DAMPs, in HD patients.
  • To assess serum levels of interleukin-6 (IL-6), a marker of inflammation, in HD patients.
  • To investigate the relationship between cytochrome c and IL-6 in HD patients.

Main Methods:

  • Enzyme-linked immunosorbent assay (ELISA) was used to measure serum cytochrome c and IL-6.
  • The study included 34 patients undergoing hemodialysis and 20 healthy controls.

Main Results:

  • Serum cytochrome c levels were significantly higher in HD patients compared to controls (1392.88 ± 905.24 pg/mL vs. 212.95 ± 91.71 pg/mL).
  • Serum IL-6 levels were also significantly elevated in HD patients compared to controls (50.32 ± 35.89 pg/mL vs. 14.27 ± 6.83 pg/mL).
  • A positive correlation was observed between serum cytochrome c and IL-6 levels in HD patients (r = 0.458).

Conclusions:

  • Both circulating cytochrome c and IL-6 are markedly increased in hemodialysis patients.
  • Elevated cytochrome c levels are positively associated with increased IL-6 levels in HD patients, suggesting a link between mitochondrial damage and inflammation.

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