![]() ![]() NAAA catalyzes the deactivating hydrolysis of palmitoylethanolamide, a lipid-derived agonist of the transcriptional regulator of cellular metabolism, peroxisome proliferator-activated receptor-α (PPAR-α). Here we show that N-acylethanolamine acid amidase (NAAA) is a critical control point in the progression to pain chronicity, which can be effectively targeted by small-molecule therapeutics that inhibit this enzyme. Understanding the molecular events leading to its emergence is necessary to discover disease-modifying therapies. ![]() ![]() ![]() Chronic pain affects 1.5 billion people worldwide but remains woefully undertreated.
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