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The kinase mTOR regulates the differentiation of helper T cells through the selective activation of signaling by mTORC1 and mTORC2

These factors disrupt intercellular communication within the corpus cavernosum and reduce nitric oxide (NO) bioavailability, thereby exacerbating endothelial dysfunction and ultimately impairing erectile function[65]

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291 In the absence of TSC2, hyperactivated mTORC1 phosphorylates S6K1 and inactivates GSK3, leading to the dephosphorylation and activation of glycogen synthase, which promotes glycogen synthesis

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