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Ratiometric Biosensors that Measure Mitochondrial Redox State and ATP in Living Yeast Cells
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Mitochondrial redox system, dynamics, and dysfunction in lung inflammaging and COPD.

Chad A Lerner1, Isaac K Sundar1, Irfan Rahman1

  • 1Department of Environmental Medicine, Lung Biology and Disease Program, University of Rochester Medical Center, Rochester, NY, USA.

The International Journal of Biochemistry & Cell Biology
|July 31, 2016
PubMed
Summary
This summary is machine-generated.

Mitochondrial dysfunction, driven by stress and impacting key cellular processes, contributes to chronic obstructive pulmonary disease (COPD) pathogenesis. This review explores how mitochondrial damage and inflammation drive COPD development and exacerbations.

Keywords:
Cellular senescenceDAMPsInflammationMitophagyOxidative phosphorylationRedoxTelomere

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Area of Science:

  • Mitochondrial biology
  • Cellular stress response
  • Pulmonary medicine

Background:

  • Mitochondrial homeostasis is crucial for cellular function and is disrupted by various endogenous and environmental stressors.
  • Stressors increase reactive oxygen species, inflammation, and cellular senescence (inflammaging), often through mitochondrial damage-associated molecular patterns (DAMPs).
  • These cellular events are implicated in the pathogenesis of chronic obstructive pulmonary disease (COPD) and its exacerbations.

Purpose of the Study:

  • To review the primary mitochondrial quality control mechanisms affected by oxidative stress.
  • To elucidate the role of mitochondria in inflammation and cellular senescence.
  • To explain how mitochondrial dysfunction contributes to COPD pathogenesis and exacerbations.

Main Methods:

  • Literature review focusing on mitochondrial function, oxidative stress, inflammation, cellular senescence, and COPD.
  • Analysis of the interplay between mitochondrial damage-associated molecular patterns (DAMPs) and disease pathogenesis.
  • Synthesis of evidence linking mitochondrial dysfunction to COPD development and exacerbations.

Main Results:

  • Oxidative stress significantly impacts mitochondrial redox systems, oxidative phosphorylation, biogenesis, and mitophagy.
  • Mitochondria play a key role in initiating and propagating inflammatory responses and cellular senescence.
  • Mitochondrial dysfunction, driven by pathogenic stimuli, is a critical factor in COPD pathogenesis.

Conclusions:

  • Mitochondrial quality control mechanisms are vital for preventing cellular damage and disease.
  • Dysfunctional mitochondria contribute significantly to the inflammatory and senescent environment characteristic of COPD.
  • Targeting mitochondrial pathways may offer therapeutic strategies for COPD and its exacerbations.