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Summary of major findings. After CH, ET-1 receptor (ETR) stimulation and membrane stretch resulting from increases in intraluminal pressure activate EGFR via Src-dependent MMP activation. EGFR signaling leads to Rho kinase (ROK)-dependent Ca2+ sensitization through NADPH oxidase 2 (NOX2)-derived O2−. Our findings support a role for this signaling mechanism in the development of pulmonary hypertension.
