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The phase of breaking through the mucosal wall, which is still a difficult task when administered by inhalation, can be avoided with intravenous administration for the treatment of respiratory disorders [25, 27]
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eNAD can bind different subtypes of purinergic P2 receptors, including P2Y11, leading to the opening of L-type Ca 2+ channels and activation of a cAMP/cADPR/[Ca 2+ ]i signaling cascade, ultimately causing increased proliferation and migration (57)
