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In PAH pulmonary arterial smooth muscle cells, TRPC3 participates in the aberrant store-operated Ca<jats:sup>2+<\/jats:sup> entry contributing to their pathological cell phenotypes (exacerbated proliferation, enhanced migration, apoptosis resistance, and vasoconstriction). Pharmacological in vivo inhibition of TRPC3 reduces the development of experimental PAH. 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