Hypoxia is a common underlying condition of many disease states. Hypoxia can occur with ischemia, a lack of blood flow to tissues, or independent of ischemia as in acute lung injury, anemia, and carbon monoxide poisoning. Hypoxia may be observed in patients with diseases such as obstructive sleep apnea, cerebrovascular diseases, systemic hypertension, cardiovascular diseases, chronic obstructive pulmonary disease (COPD), pulmonary hypertension and congestive heart failure (CHF), inflammatory disease states, and acute and chronic renal diseases. In the past decade, research has shown hypoxic signaling to be involved in a range of responses from adaptation of the body to reduced oxygen to pathogenesis of disease. Hypoxic signaling intermediates orchestrate a whole host of responses from angiogenesis, glycolysis, and erythropoiesis to inflammation and remodeling, which could be beneficial or harmful to the hosting organ. The length of exposure to low oxygen pressure as well as the existing signaling pathways within different cells dictates their benefit or disadvantage from hypoxic signaling. Therefore, activation or inhibition of hypoxic intermediates could serve as novel therapeutic strategies. In this chapter, we review the role of hypoxic signaling in neurodegenerative, inflammatory, and renal disease states and the emerging therapeutic approaches involving hypoxic signaling.
Part of the book: Hypoxia and Human Diseases