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Cited by 511

The DOI matches its Crossref record; 11 of the 11 references it cites were found in a registry or an index.

Expression of hypoxia-inducible factor 1: mechanisms and consequences

Open access
Semenza, Gregg L·2000·Biochemical Pharmacology

Abstract

Hypoxia-inducible factor 1 (HIF-1) is a basic-helix-loop-helix transcription factor that plays essential roles in mammalian development and physiology. HIF-1 is a heterodimer composed of HIF-1alpha and HIF-1beta subunits. The expression and activity of the HIF-1alpha subunit are tightly regulated by cellular O2 concentration. Under hypoxic conditions, HIF-1 activates the transcription of genes encoding erythropoietin, glucose transporters, glycolytic enzymes, vascular endothelial growth factor, and other genes whose protein products increase O2 delivery or facilitate metabolic adaptation to hypoxia. HIF-1 is essential for embryonic vascularization and survival, neovascularization in ischemic myocardium, hypoxia-induced pulmonary vascular remodeling, and tumor vascularization. HIF-1alpha is overexpressed in the majority of common human cancers and their metastases, due to the presence of intratumoral hypoxia and as a result of mutations in genes encoding oncoproteins and tumor suppressors. Pharmacologic manipulation of HIF-1 levels may provide a novel therapeutic approach to diseases that represent the most common causes of mortality in Western society, including cancer, chronic lung disease, and myocardial ischemia.

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Metadata

Authors
Semenza, G. L.
Venue
Biochemical Pharmacology
Publisher
Elsevier BV
Published
2000-01
Volume
59
Issue
1
Pages
47-53
ISSN
0006-2952 (ISSN-L)
OpenAlex
W2077688090
Cited by
511
References
11
FWCI
10.70
Type
journal article
Language
en
Open access
hybrid

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CoChat. (2026). Citation check: Expression of hypoxia-inducible factor 1: mechanisms and consequences. https://app.cochat.ai/papers/10.1016/s0006-2952(99)00292-0
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Semenza, G. L. (2000). Expression of hypoxia-inducible factor 1: mechanisms and consequences. Biochemical Pharmacology. https://doi.org/10.1016/s0006-2952(99)00292-0

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