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The stimulation of thrombosis by hypoxia.

08:00 EDT 15th July 2019 | BioPortfolio

Summary of "The stimulation of thrombosis by hypoxia."

Thrombus formation is increased under conditions of hypoxia in animal models of thrombosis and in human populations, but current therapies for thrombosis do not directly target hypoxia-responsive signaling pathways. The vascular response to hypoxia is controlled primarily by the hypoxia-inducible transcription factors (HIFs), whose target genes include several factors that regulate thrombus formation. In this article, we review the HIF-dependent and HIF-independent signaling pathways that regulate thrombus formation under hypoxic conditions. A better understanding of hypoxia-induced thrombus formation could lead to the development of novel prophylactic therapies for thrombosis.

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This article was published in the following journal.

Name: Thrombosis research
ISSN: 1879-2472
Pages: 77-83

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Medical and Biotech [MESH] Definitions

Dioxygenase enzymes that specifically hydroxylate a PROLINE residue on the HYPOXIA-INDUCIBLE FACTOR 1, ALPHA SUBUNIT. They are OXYGEN-dependent enzymes that play an important role in mediating cellular adaptive responses to HYPOXIA.

Stimulation of the brain, which is self-administered. The stimulation may result in negative or positive reinforcement.

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Localized reduction of blood flow to brain tissue due to arterial obstruction or systemic hypoperfusion. This frequently occurs in conjunction with brain hypoxia (HYPOXIA, BRAIN). Prolonged ischemia is associated with BRAIN INFARCTION.

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