PLA2 activity is stimulated by microbial products, thrombin, immunoglobulins, etc., whereas anti-inflammatory glucocorticoids are known to inhibit it ( Engelking, 2015). AA is first released by the action of phospholipase A2 (PLA2) from plasma membranephospholipids, which acts at the sn-2 position of the phospholipid backbone ( Engelking, 2015 Hanna and Hafez, 2018). Some of the therapeutic approaches targeting COX-2 and mTOR in AD and cancer are also discussed.Ĭyclooxygenase-2 (COX-2) is an isoform of the cyclooxygenase enzyme family, along with COX-1 and COX-3, which are involved in the synthesis of prostanoids (eicosanoid sub-class) from an essential fatty acid, namely arachidonic acid (AA). ![]() They are also known to act in cooperation in many different cancers and thus, their role together in normal cellular functions as well as AD has been explored in this review. COX-2 and mTOR are both involved in environmental sensing, growth, and metabolic processes of the cell. Mammalian/mechanistic target of rapamycin (mTOR) has been considered as a hub which integrates multiple signaling cascades, some of which are also involved in AD progression. However, an increasing number of reports point to much more complex roles of COX-2 in AD. COX-2 was traditionally viewed to be expressed only under pathological conditions and to have detrimental effects in AD pathophysiology and neurodegeneration. COX-1 and COX-2 have been widely studied in order to explore and understand their involvement in Alzheimer’s disease (AD), a progressive neuroinflammatory dementia. COX exists in three isoforms: COX-1, 2, and 3.
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