gsk1278863 and Reperfusion-Injury

Oxygen is vital to mammalian survival. Oxygen deprivation, defined as hypoxia, elicits adaptive responses in cells and tissues, a process regulated by proteins known as hypoxia-inducible factors (HIF). Animal studies have provided compelling data to demonstrate a pivotal role for the HIF pathway in the pathogenesis of acute kidney injury (AKI) that have led to initial human clinical trials examining this pathway in ischemia-reperfusion injury in various organ systems, including the kidney. HIF are master regulators and mediate adaptive responses to low oxygen in tissues and cells. This review will summarize recent key advances in the field highlighting preclinical and clinical studies relevant to the HIF pathway in the pathophysiology of AKI.

Topics: Acetazolamide; Acute Kidney Injury; Adaptation, Physiological; Altitude; Animals; Barbiturates; Basic Helix-Loop-Helix Transcription Factors; Cell Hypoxia; Clinical Trials, Phase II as Topic; Gene Expression Regulation; Glycine; Humans; Hypoxia-Inducible Factor 1; Hypoxia-Inducible Factor-Proline Dioxygenases; Intercellular Signaling Peptides and Proteins; Kidney; Mice; Rats; Reactive Oxygen Species; Reperfusion Injury; Transcription Factors; Transcription, Genetic; Von Hippel-Lindau Tumor Suppressor Protein