Key result
VIP replacement attenuates spontaneous pulmonary arterial hypertension and RV hypertrophy in VIP-deficient mice.
Why the study?
Vasoactive intestinal peptide (VIP) is absent in pulmonary arteries from patients with idiopathic pulmonary arterial hypertension, but the role of VIP gene deletion in PAH development was unclear.
Does targeted deletion of the VIP gene lead to pulmonary arterial hypertension and vascular remodeling in male mice, and can VIP treatment attenuate these effects?
Does targeted deletion of the VIP gene lead to pulmonary arterial hypertension and vascular remodeling in male mice, and can VIP treatment attenuate these effects?
VIP knockout mice develop spontaneous pulmonary arterial hypertension and right ventricular remodeling that can be attenuated with VIP treatment, highlighting VIP's potential role in PAH pathogenesis and therapy.
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VIP knockout induces PAH-like changes in mice; leaves open whether VIP modulation could benefit human PAH.
Said et al. (2007) studied Pulmonary arterial hypertension. Targeted deletion of the VIP gene vs. Wild-type control mice was evaluated on Evidence of PAH, right ventricular hypertrophy, and pulmonary vascular remodeling. Targeted deletion of the VIP gene in male mice led to spontaneous moderately severe pulmonary arterial hypertension and right ventricular hypertrophy, which were attenuated by a 4-week VIP treatment.
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