Skip to main content
Fig. 2 | Journal of Neuroinflammation

Fig. 2

From: Arachidonic acid-derived lipid mediators in multiple sclerosis pathogenesis: fueling or dampening disease progression?

Fig. 2

Schematic overview of the molecular signalling that leads to AA hydrolysis from glycerophospholipids in cellular membranes of the Golgi system and the nuclear envelope. Environmental stimuli (e.g., pro-inflammatory cytokines) that either activate the MAPK-signalling pathway (1) or raise intracellular Ca2+ levels (2) result in the phosphorylation of group IVA cytosolic phospholipase A2 (cPLA2-α) (3). This results in the translocation of cPLA2-α towards the cellular membranes of the Golgi system and the nuclear envelope, where it interacts with esterified AA incorporated in glycerophospholipids, which will make AA accessible for further metabolism (4). Enzymes with oxidative properties, such as cyclooxygenases (COXs) and lipoxygenases (LOXs), that reside in these cellular membranes can interact with this hydrolyzed AA and convert it into a variety of bioactive LMs (5). *for simplicity, only MAPK without further upstream signalling is shown

Back to article page