Journal
TRENDS IN PHARMACOLOGICAL SCIENCES
Volume 36, Issue 6, Pages 395-405Publisher
ELSEVIER SCIENCE LONDON
DOI: 10.1016/j.tips.2015.03.006
Keywords
arginase; vascular dysfunction; neurodegeneration; polyamine; oxidative stress; nitric oxide; peroxynitrite; superoxide
Categories
Funding
- Department of Veterans Affairs, Veterans Health Administration, Office of Research and Development
- Vision Discovery Institute at Georgia Regents University
- VA Research Career Scientist Award
- VA Merit Review Award
- Public Health Service [EY011766, HL070215]
- American Heart Association
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Arginase has roots in early life-forms. It converts L-arginine to urea and ornithine. The former provides protection against NH3; the latter serves to stimulate cell growth and other physiological functions. Excessive arginase activity in mammals has been associated with cardiovascular and nervous system dysfunction and disease. Two relevant aspects of this elevated activity may be involved in these disease states. First, excessive arginase activity reduces the supply of L-arginine needed by nitric oxide (NO) synthase to produce NO. Second, excessive production of ornithine leads to vascular structural problems and neural toxicity. Recent research has identified inflammatory agents and reactive oxygen species (ROS) as drivers of this pathologic elevation of arginase activity and expression. We review the involvement of arginase in cardiovascular and nervous system dysfunction, and discuss potential therapeutic interventions targeting excess arginase.
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