Morphine for the Treatment of Pain in Sickle Cell Disease

Figure 1

Proposed model of morphine-induced signaling leading to organ damage. Morphine signaling via cyclooxygenase-2 (COX-2), platelet-derived growth factor-β (PDGFR-β), and toll-like receptor 4 (TLR4) may underlie the morphine-induced hyperalgesia and tolerance via its action on the central nervous system (CNS); promote endothelial dysfunction and associated retinopathy, lung injury, pulmonary arterial hypertension, and stroke; and contribute to renal dysfunction in sickle cell disease.