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Proposed mechanism by which CH augments depolarization-induced pulmonary vasoconstriction. CH augments depolarization-induced activation of an EGFR/NOX2/ROK signaling axis and resultant vasoconstriction by coupling membrane depolarization to EGFR stimulation, and by reducing membrane cholesterol content. Cholesterol inhibits this signaling pathway downstream of EGFR. NOX2 = NADPH oxidase 2; ROK = RHO-associated protein kinase.
