HIF-1: mediator of physiological and pathophysiological responses to hypoxia.
By G. Semenza. Journal of applied physiology, 2000
1,863 citations recorded by the source corpus.
Subfields: Cancer Research, Genetics, Physiology
View Paper: https://www.semanticscholar.org/paper/ab5038de9bdcaa849c9eea878a637f182160df92
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Citations in the corpus
- Free radicals and antioxidants in normal physiological functions and human disease. (2007, background): “HIF-1 is expressed and HIF-1 accumulated only in hypoxic cells (Semenza, 2000).”
- Mechanisms of neuronal cell death in ischemic stroke and their therapeutic implications (2021, background): “HIF‐1, which consists of an oxygen‐regulated subunit HIF‐1α and a constitutively expressed subunit HIF‐1β,(142) is essential for maintaining oxygen levels in mammalian cells.(143,144) It is reported to be activated during ischemia in response to hypoxia(145) and can induce the transcription of more ”
- Oxygen sensing by mitochondria at complex III: the paradox of increased reactive oxygen species during hypoxia (2006, background): “Hypoxia-inducible factor is a heterodimeric complex comprised of an oxygenregulatedα subunit (HIF-α) and a constitutively expressed β subunit, also referred to as the arylhydrocarbon receptor nuclear translocator (ARNT; Semenza, 2000).”
- Regulation of retinal blood flow in health and disease. (2008, background): “There is compelling evidence that, during retinal and choroidal neovascularization and formation of diabetic macular edema, hypoxia strongly induces VEGF expression through stabilization of transcription factor HIF-1 (hypoxia-inducible factor-1) (Semenza, 2000; Pages and Pouyssegur, 2005; Arjamaa an”
- Chapter 3 – A Profile of the Metabolic Responses to Anoxia in Marine Invertebrates (2002, background): “For example, HIF-1 mediates the increased synthesis of glycolytic enzymes to enhance the capacity for fermentative ATP production while at the same time stimulating red blood cell production (via induction of erythropoeitin) and the proliferation of capillaries (via induction of vascular endothelial”
- Hypoxia, Clonal Selection, and the Role of HIF-1 in Tumor Progression (2000, background): “The developmental and physiological roles of these fac- tors have been reviewed elsewhere recently (Crews and Fan, 1999; Semenza, 1999, 2000).”
- Functional classification of interferon‐stimulated genes identified using microarrays (2001, background): “The HIF1a protein stimulates transcription of genes that mediate the intracellular response to anoxia and induces angiogenesis [68, 69].”
- Retinoid-related orphan receptors (RORs): critical roles in development, immunity, circadian rhythm, and cellular metabolism (2009, background): “Hypoxia is important in normal physiology and in several pathologies, including ischemia, stroke, heart attack, chronic kidney disease, and cancer progression [Pouyssegur et al., 2006; Semenza, 2000].”
- Genetic adaptation to high altitude in the Ethiopian highlands (2012, background): “During fetal development, the liver is the primary source of erythropoietin, and HIF regulates the production of erythropoietin, which is required for red blood cell production [31].”
- HIF-1 and human disease: one highly involved factor. (2000, methodology): “Experimental data (for review, see Semenza 2000b) suggest the following model: Increased VEGF expression is required to initiate and sustain tumor angiogenesis.”
- Obesity in C57BL/6J mice is characterized by adipose tissue hypoxia and cytotoxic T-cell infiltration (2008, background): “Results: We determined that obesity in male C57BL/6J mice is associated with increased expression of HIF (hypoxia-inducible factor) isoforms and GLUT-1, and that white adipose tissue hypoxia was present in the obese mice. Immunohistochemistry revealed hypoxic areas to colocalize predominantly with F”
- Chapter 20 Antioxidant defenses and animal adaptation to oxygen availability during environmental stress (2001, background): “These mechanisms might include erythropoietin-like heme proteins and transcription factors such as Fos, AP-1, NFkappa-B and hypoxia-inducible factor-1 (HIF-1) (Hochachka et al., 1996, 1997; Walton et al., 1999; Zhu and Bunn, 1999; Semenza, 2000).”