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. Author manuscript; available in PMC: 2015 Apr 1.
Published in final edited form as: Neuropharmacology. 2013 Dec 4;79:249–261. doi: 10.1016/j.neuropharm.2013.11.022

Fig. 11.

Fig. 11

Proposed mechanisms of telmisartan neuroprotection. Glutamate stimulates NMDA receptors and induces neuronal injury by increasing apoptosis and inflammation. Mechanisms include increased AT1 receptor expression, inhibition of the anti-apoptotic Akt pathway, and ERK1/2 stimulation. Telmisartan reduces glutamate-induced apoptosis and inflammation in CGCs. Telmisartan neuroprotection is the result of dual AT1 receptor blockade and PPARγ activation, decreasing apoptosis and inflammation by mechanisms involving a reduction of glutamate-induced alterations in the Akt/GSK-3β and ERK1/2 pathways.