The DOI matches its Crossref record; 32 of the 33 references it cites were found in a registry or an index.
Hypoxia, HIF-1, and the Pathophysiologi of Common Human Diseases
Abstract
Hypoxia plays a fundamental role in the pathophysiology of common causes of mortality, including ischemic heart disease, stroke, cancer, chronic lung disease, and congestive heart failure. In these disease states, hypoxia induces changes in gene expression in target organs that either fail to result in adequate adaptation or directly contribute to disease pathogenesis. Hypoxia-inducible factor 1 (HIF-1) is a transcriptional activator that is expressed in response to cellular hypoxia and mediates multiple cellular and systemic homeostatic responses to hypoxia. Recent studies have provided evidence that important pathophysiological responses to hypoxia in pulmonary hypertension, myocardial ischemia, and cancer are mediated by HIF-1. Pharmacologic and gene therapy strategies designed to modulate HIF-1 activity may represent a novel and effective therapeutic approach to these common disorders.
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“However, overexpression of catalase localized to mitochondria increased median life span in mice by 5 months (280).”
From Mitochondrial reactive oxygen species production in excitable cells: Modulators of mitochondrial and cell function (2009) · cites this paper as [280]
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Metadata
- Authors
- Semenza, G. L., Agani, F., Feldser, D., Lyer, N., Kotch, L., Laughner, E., & Yu, 1.
- Affiliations
- Johns Hopkins University (US)
- Venue
- Advances in Experimental Medicine and Biology
- Publisher
- Kluwer Academic Publishers
- Published
- 2006-03-05
- Volume
- 475
- Pages
- 123-130
- OpenAlex
- W2116889376
- Cited by
- 241
- References
- 33
- Citations by year
- 2026: 1 · 2025: 3 · 2024: 6 · 2023: 4 · 2022: 9 · 2021: 9 · 2020: 4 · 2019: 5 · 2018: 3 · 2017: 8 · 2016: 12 · 2015: 9 · 2014: 5 · 2013: 13 · 2012: 11
- FWCI
- 40.79
- Type
- book chapter
- Language
- en
- Open access
- closed
- Locations
- Kluwer Academic Publishers eBooks (publishedVersion)
- PubMed (publishedVersion)
- Funders
- American Heart Association
- Johns Hopkins University
- National Institutes of Health (5r01dk039869-16)
- National Heart, Lung, and Blood Institute (R01HL55338, R01HL055338)
- National Institute of Diabetes and Digestive and Kidney Diseases (R01 DK39869)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Hypoxia, and Metabolism
- Health Sciences › Medicine › Hematology › Erythropoietin and Anemia Treatment
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Angiogenesis and VEGF in Cancer
- Keywords
- hypoxia, HIF-1, ischemic heart disease, stroke, cancer, chronic lung disease, congestive heart failure, pulmonary hypertension, myocardial ischemia, gene expression, transcriptional regulation, gene therapy
- MeSH terms
- Animals, Hypoxia, DNA-Binding Proteins, Embryonic and Fetal Development, Humans, Hypertension, Pulmonary, Lymphokines, Myocardial Revascularization, Neoplasms, Nuclear Proteins, Transcription Factors, Genetic Therapy, Gene Expression, Endothelial Growth Factors, Mice, Knockout, Vascular Endothelial Growth Factors, Vascular Endothelial Growth Factor A, Mice, Hypoxia-Inducible Factor 1, Hypoxia-Inducible Factor 1, alpha Subunit
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