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Fig. 2 | Journal of Cannabis Research

Fig. 2

From: Role of the endocannabinoid system in the pathophysiology of endometriosis and therapeutic implications

Fig. 2

The endocannabinoid system signaling cascade. Arachidonoylethanolamine (AEA) and 2-arachidonoylglycerol (2-AG) are biosynthesized by N-acylphosphatidylethanolamine phospholipase D (NAPE-PLD) and diacylglycerol lipase (DAGL), respectively. Fatty acid amide hydrolase (FAAH) and MAGL are the metabolizing enzymes that degrade AEA to produce arachidonic acid (AA) and ethanolamine (ETA), and 2-AG to AA and glycerol. AEA and 2-AG are transported in and out of a cell through the putative endocannabinoid membrane transporters (EMTs). AEA and 2-AG bind to G protein-coupled receptors (GRPs), such as cannabinoid receptors 1 (CB1) and 2 (CB2), at varying affinities and to a lesser extent with the orphan GPR and transient receptor potential (TRP) channels. The endocannabinoid system (ECS) mainly targets the protein kinase A (PKA) signaling cascade via inhibition of adenylyl cyclase (AC)-cyclic adenosine monophosphate (AMP) that has direct inhibitory effects on β-catenin which affects epithelial-mesenchymal transition. Activation of the mitogen-activated protein kinase signaling cascades, such as extracellular signal-regulated kinase ½ (ERK ½), protein kinase B or Akt, phosphatidylinositol-3-kinase (PI3K), mitogen-activated protein kinase (MEK1/2), and mammalian target of rapamycin (mTOR), is involved in cellular processes such as autophagy, apoptosis, cell cycle, and proliferation

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