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Accumulation of damaged mitochondria in alveolar macrophages with reduced OXPHOS related gene expression in IPF

Eliza Tsitoura1, Eirini Vasarmidi1,2, Eleni Bibaki1

  • 1Department of Respiratory Medicine, Laboratory of Molecular and Cellular Pneumonology, Medical School, University of Crete, Heraklion, Crete, Greece.

Respiratory Research
|November 29, 2019
PubMed
Abstract

Insights

Mitochondria in alveolar macrophages are dysfunctional in idiopathic pulmonary fibrosis (IPF), showing morphological defects and impaired homeostasis. This dysfunction is linked to increased mitochondrial reactive oxygen species (mtROS) and not compensated by autophagy.

Area of Science:

  • Cellular Biology
  • Aging Research
  • Pulmonary Medicine

Background:

  • Mitochondrial dysfunction is a hallmark of aging and implicated in lung fibrosis.
  • Alveolar macrophages (AMs) in idiopathic pulmonary fibrosis (IPF) may exhibit altered mitochondrial homeostasis.

Purpose of the Study:

  • To investigate mitochondrial homeostasis and function in AMs from IPF patients.
  • To explore the relationship between mitochondrial health, aging, and lung function decline in IPF.

Main Methods:

  • Analysis of bronchoalveolar lavage (BAL) samples from 52 IPF patients and 19 healthy controls.
  • Assessment of mitochondrial reactive oxygen species (mtROS), morphology, gene expression, autophagy, and mitophagy.

Main Results:

  • IPF AMs displayed mitochondrial morphological defects and reduced expression of key homeostasis regulators (PINK1, PARK2, NRF1).
  • Elevated mtROS levels in IPF correlated with reduced oxidative phosphorylation gene expression and were associated with age and declining lung function.
  • Increased damaged mitochondria in IPF AMs were not accompanied by enhanced macroautophagy or mitophagy.

Conclusions:

  • Mitochondrial homeostasis is perturbed in alveolar macrophages of IPF patients.
  • Dysfunctional mitochondria and impaired clearance mechanisms may contribute to IPF pathogenesis.
Keywords:
Alveolar macrophagesAutophagyIdiopathic pulmonary fibrosisMitochondriaMitophagy

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