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Proposed molecular mechanism of eNOS stimulation after TRPV1 activation. Activation of TRPV1 increases Ca2+ influx, which in turn activates PI3K/Akt/CaMKII signaling, leading to increased TRPV1 and eNOS phosphorylation. In addition, TRPV1 may serve as a scaffold for the formation of a complex comprising Akt, AMPK, CaMKII, and eNOS. Protein interactions seem to be important in eNOS activation and NO release.
