Lung cell hypoxia: Role of mitochondrial reactive oxygen species signaling in triggering responses

Paul T. Schumacker*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

54 Scopus citations

Abstract

Lung cells experience hypoxia during development, during travel to high altitude, and in acute and chronic lung diseases. The functional responses evoked by hypoxia are diverse and generally act to protect the cells from hypoxic injury, although some lung cell responses are counterproductive because they degrade normal function of the organ. The cellular O 2 sensor responsible for many of these responses involves the mitochondrial electron transport chain. Under hypoxic conditions, increased release of reactive oxygen species from the inner mitochondrial membrane to the intermembrane space leads to the activation of transcription factors, including hypoxia-inducible factor, activation of hypoxic pulmonary vasoconstriction, activation of AMP-dependent protein kinase, and internalization of the membrane Na,K-ATPase from the basolateral membrane of alveolar epithelial cells. Although the specific targets of reactive oxygen species signals are not fully understood, this signaling pathway is critical for development and for normal lung responses in the newborn and the mature lung.

Original languageEnglish (US)
Pages (from-to)477-484
Number of pages8
JournalProceedings of the American Thoracic Society
Volume8
Issue number6
DOIs
StatePublished - Nov 1 2011

Keywords

  • Alveolar epithelium
  • Hypoxic pulmonary vasoconstriction
  • Lung injury
  • Oxygen sensing
  • Pulmonary circulation

ASJC Scopus subject areas

  • Pulmonary and Respiratory Medicine

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