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O(2) sensing in hypoxic pulmonary vasoconstriction: the mitochondrial door re-opens
Gregory B Waypa1, Paul T Schumacker
1Department of Medicine MC6026, The University of Chicago, 5841 South Maryland Avenue, Chicago, IL 60637, USA.
Respiratory Physiology & Neurobiology
|July 20, 2002
Summary
Mitochondria are key to the hypoxic pulmonary vasoconstriction (HPV) response. Two models propose either decreased or increased mitochondrial reactive oxygen species (ROS) generation under hypoxia, triggering HPV.
Area of Science:
- Physiology
- Cell Biology
- Pulmonary Medicine
Background:
- The oxygen sensor for hypoxic pulmonary vasoconstriction (HPV) remains elusive after 50 years.
- Mitochondria are increasingly implicated in initiating the pulmonary artery constriction response to low oxygen.
- Two distinct models propose how mitochondria mediate HPV.
Purpose of the Study:
- To review and compare two contrasting models of mitochondrial function in HPV.
- To elucidate the role of mitochondria in sensing oxygen levels during HPV.
Main Methods:
- Review of existing literature on mitochondrial function and HPV.
- Analysis of proposed molecular mechanisms in two disparate models of HPV.
Main Results:
- Model 1: Hypoxia inhibits mitochondrial electron transport, decreasing reactive oxygen species (ROS) and activating a redox-sensitive pathway.
- Model 2: Hypoxia paradoxically increases mitochondrial ROS generation, activating an oxidant-sensitive pathway.
Conclusions:
- Mitochondria are central to HPV, but their precise role in oxygen sensing is debated.
- Further research is needed to reconcile the opposing models of mitochondrial involvement in HPV.