Key result
Pharmacological in vivo inhibition of TRPC3 reduces the development of experimental pulmonary arterial hypertension, suggesting it as a potential innovative treatment.
Why the study?
Does pharmacological inhibition of TRPC3 reduce the development of experimental pulmonary arterial hypertension?
Does pharmacological inhibition of TRPC3 reduce the development of experimental pulmonary arterial hypertension?
Inhibition of TRPC3 reduces the development of experimental pulmonary arterial hypertension, suggesting it could be an innovative treatment target.
TRPC3 inhibition merits investigation as a PAH target; leaves open clinical translation pending human studies.
TRPC3 is increased in human and experimental pulmonary arterial hypertension (PAH). In PAH pulmonary arterial smooth muscle cells, TRPC3 participates in the aberrant store-operated Ca 2+ 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. Even if other TRPC acts on PAH development, our results prove that TRPC3 inhibition could be considered as an innovative treatment for PAH.
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Masson et al. (2023) studied Pulmonary arterial hypertension. TRPC3 inhibition was evaluated on Development of experimental PAH and pathological cell phenotypes. Pharmacological in vivo inhibition of TRPC3 reduces the development of experimental pulmonary arterial hypertension, suggesting it as a potential innovative treatment.
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