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Cited by 1,159

The DOI matches its Crossref record; 59 of the 59 references it cites were found in a registry or an index.

Oxygen Sensing, Hypoxia-Inducible Factors, and Disease Pathophysiology

Semenza, Gregg L.·2014·Annual Review of Pathology: Mechanisms of Disease

Abstract

Hypoxia-inducible factors (HIFs) are transcriptional activators that function as master regulators of oxygen homeostasis, which is disrupted in disorders affecting the circulatory system and in cancer. The role of HIFs in these diseases has been elucidated by clinical studies and by analyses of mouse models. HIFs play a protective role in the pathophysiology of myocardial ischemia due to coronary artery disease, limb ischemia due to peripheral arterial disease, pressure-overload heart failure, wound healing, and chronic rejection of organ transplants. In contrast, HIFs contribute to the pathogenesis of pulmonary arterial hypertension, systemic hypertension associated with sleep apnea, ocular neovascularization, hereditary erythrocytosis, and cancer.

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Crossref · 10.1146/annurev-pathol-012513-104720

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Metadata

Authors
Semenza, G. L.
Venue
Annual Review of Pathology: Mechanisms of Disease
Published
2014-01-24
Volume
9
Issue
1
Pages
47-71
ISSN
  • 1553-4006 (ISSN-L)
  • 1553-4014
OpenAlex
W2137465719
Cited by
1,159
References
59
FWCI
5.15
Type
journal article
Language
en
Open access
closed

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CoChat. (2026). Citation check: Oxygen Sensing, Hypoxia-Inducible Factors, and Disease Pathophysiology. https://app.cochat.ai/papers/10.1146/annurev-pathol-012513-104720
The paper
Semenza, G. L. (2014). Oxygen Sensing, Hypoxia-Inducible Factors, and Disease Pathophysiology. Annual Review of Pathology: Mechanisms of Disease. https://doi.org/10.1146/annurev-pathol-012513-104720

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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.

Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.