Thromb Haemost 2007; 97(05): 774-787
DOI: 10.1160/TH06-12-0744
Review Article
Schattauer GmbH

Cellular and molecular mechanisms of hypoxia-inducible factor driven vascular remodeling

Jörg Hänze
1  University of Giessen Lung Center (UGLC), Medical Clinic II/V, Giessen, Germany
,
Norbert Weissmann
1  University of Giessen Lung Center (UGLC), Medical Clinic II/V, Giessen, Germany
,
Friedrich Grimminger
1  University of Giessen Lung Center (UGLC), Medical Clinic II/V, Giessen, Germany
,
Werner Seeger
1  University of Giessen Lung Center (UGLC), Medical Clinic II/V, Giessen, Germany
,
Frank Rose
2  Department of Radiotherapy and Radiooncology, University of Marburg, Marburg, Germany
› Author Affiliations
Financial support: Studies on this subject performed in our laboratory were supported by the Deutsche Forschungsgemeinschaft SFB 547 projects.
Further Information

Publication History

Received 30 December 2006

Accepted after resubmission 01 March 2007

Publication Date:
24 November 2017 (online)

Summary

Hypoxia-inducible factor (HIF) is an oxygen-dependent transcription factor that activates a diverse set of target genes, the products of which are involved in adaptive processes to hypoxia. Employing genetic manipulation of HIF expression, in-vivo and cellular studies have focused on HIF as a crucial factor affecting hypoxia-induced vascular remodeling.Vascular remodeling comprises processes which establish and improve blood vessel supply such as vasculogenesis, angiogenesis and arteriogenesis. These processes are observed during ontogenesis, tumor progression, ischemic disease or physical training. Furthermore, under hypoxic conditions, a pulmonary-specific type of vascular remodeling called pulmonary arterial remodeling occurs that is characterized by thickening of the vessel wall with a concomitant reduction in the vessel lumen area, thereby limiting blood flow.This response results in pulmonary hypertension with right ventricular hypertrophy, a lethal disease. In this review, we summarize and discuss mechanisms by which HIF interferes with the different vascular remodeling processes.