Figure 5.

Proposed pathway of hyperhomocysteinemia-induced podocyte injury leading to glomerulopathy and role of anandamide and prostamide E2. High homocysteine levels either directly or indirectly through increased NADPH oxidase activity and secondary production of ROS increases NALP3 inflammasome assembly and activation. The resulting activation of caspase-1 and conversion of proIL-1β into IL-1β produces a pro-inflammatory state that injures podocytes and results in podocyte dysfunction. Both AEA and PE2 have inhibitory effects on hyperhomocysteinemia-induced NALP3 inflammasome activation and possess anti-inflammatory activity.