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Related Experiment Video

Updated: May 31, 2026

Isolation and In Vitro Culture of Murine and Human Alveolar Macrophages
09:09

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Published on: April 20, 2018

HIF-1α and HIF-2α differentially regulate alveolar macrophage maturation and function.

Elena Priego1, Irene Adan-Barrientos2, Ruth Conde-Garrosa3

  • 1Centro Nacional de Investigaciones Cardiovasculares Carlos III, 28029 Madrid, Spain; Escuela de Doctorado, Universidad Autónoma de Madrid, 28049 Madrid, Spain; Facultad de Negocios y Tecnología, Universidad Alfonso X el Sabio (UAX), Villanueva de la Cañada, 28691 Madrid, Spain.

Cell Reports
|May 28, 2026
PubMed
Summary
This summary is machine-generated.

Hypoxia-inducible transcription factor (HIF) subunits differentially regulate alveolar macrophage (AM) maturation. HIF inactivation is crucial for AM function in high-oxygen lung environments, with HIF-2α a potential therapeutic target for lung diseases.

Keywords:
Alveolar MacrophageCP: ImmunologyCP: MetabolismHIFglycolysismitochondrial respirationself-renewalsurfactant oxidation

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Area of Science:

  • Pulmonary immunology
  • Cellular metabolism
  • Molecular biology

Background:

  • Alveolar macrophages (AMs) are crucial immune cells in the lung's high-oxygen environment.
  • The Von Hippel-Lindau protein (pVHL) targets hypoxia-inducible transcription factor (HIF) subunits for degradation.
  • Previous work indicated Vhl-deficient AMs exhibit immature phenotypes and impaired function.

Purpose of the Study:

  • To define the specific roles of HIF-1α and HIF-2α isoforms in regulating AM maturation and function.
  • To investigate the metabolic reprogramming driven by HIF isoforms in AMs.
  • To assess the therapeutic potential of targeting HIF-2α in lung disease models.

Main Methods:

  • Genetic manipulation of Vhl and HIF isoforms in mouse AMs.
  • Analysis of AM maturation, self-renewal, and metabolic pathways (glycolysis, fatty acid oxidation).
  • Utilizing a mouse model of pulmonary alveolar proteinosis to evaluate AM function in vivo.

Main Results:

  • Expression of either HIF-1α or HIF-2α alone in Vhl-deficient AMs impairs terminal maturation and self-renewal.
  • Complete rescue of AM maturation and function requires deletion of both HIF-1α and HIF-2α.
  • HIF-1α promotes glycolytic reprogramming, while HIF-2α disrupts fatty acid oxidation and surfactant clearance.
  • Stabilized HIF-2α limits AMs' ability to resolve surfactant excess in a pulmonary alveolar proteinosis model.

Conclusions:

  • HIF inactivation is essential for optimal AM maturation and metabolic adaptation to the alveolar niche.
  • HIF-1α and HIF-2α possess non-redundant, isoform-specific functions in AM regulation.
  • HIF-2α represents a potential therapeutic target for conditions involving impaired surfactant clearance, such as pulmonary alveolar proteinosis.