Arachidonic acid (AA) and other 20 or 22-carbon polyunsaturated fatty
acids (PUFAs) are precursors of lipid mediators of inflammation known as
eicosanoids. These mediators are critical in disease processes and in
regulating normal cell function. Remodeling is important in maintaining
homeostasis and in regulating cell function by dictating how PUFAs are
converted to lipid mediators of inflammation. Thus, PUFA remodeling is a
critical process in the biosynthesis of a multitude of mediators, and
understanding this process will unravel better therapeutic targets for
controlling inflammatory diseases such as asthma and Alzheimer's
disease.
AA metabolism is described in an integrated context linking the
remodeling processes with the biosynthesis of mediators and diseases. By
following the movement of the substrate (AA), the volume describes how
upstream biosynthetic pathways influence the formation of lipid
mediators of inflammation, showing the metabolic interrelationship
between all AA-derived mediators.