Abstract
Lipolysis meets inflammation: arachidonic acid mobilization from fat
Highlights
Inflammation is a fundamental protective response in higher eukaryotes to a variety of external stimuli such as environmental toxins, pathogens, or allergens
The fact that cPLA2␣ deficiency leads to attenuation, but not loss, of eicosanoid production suggests that other phospholipases A2 (PLA2) contribute to relevant PLA2 activity [7, 8]
The authors show that adipose triglyceride lipase (ATGL)-mediated hydrolysis of lipid droplet (LD)-associated TGs is crucially involved in the production of nonesterified AA in mast cells (MCs) (Fig. 1)
Summary
Inflammation is a fundamental protective response in higher eukaryotes to a variety of external stimuli such as environmental toxins, pathogens, or allergens. In the classical synthesis pathway for eicosanoids, phospholipases A2 (PLA2) hydrolyze the ester bond to release AA. Group IVA PLA2 (cPLA2␣) is considered to be the primary phospholipase for AA release in mice and in humans (Fig. 1).
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