Key result
Bmpr2 ± transgenic mice are an inadequate model for studying iron deficiency in pulmonary vascular disease.
Why the study?
Bmpr2 mutations are the most common genetic cause of PAH and iron deficiency is linked to worse clinical outcomes, prompting evaluation of Bmpr2 +/- mice to model iron deficiency in pulmonary vascular disease.
Are Bmpr2 ± mice a suitable model for studying iron deficiency in pulmonary hypertension?
Are Bmpr2 ± mice a suitable model for studying iron deficiency in pulmonary hypertension?
Bmpr2 ± mice are an inadequate model for studying iron deficiency in pulmonary hypertension.
Bmpr2 ± mice are unsuitable to model iron deficiency in PAH; leaves open need for alternative preclinical models.
As bone morphogenetic protein receptor type II (Bmpr2) mutations are the most common genetic cause of pulmonary arterial hypertension (PAH), and iron deficiency (ID) is associated with worse clinical outcomes in PAH patients, we proposed to use Bmpr2 ± mice to induce a model of ID in pulmonary vascular disease. Our study shows that these transgenic mice are not a good model for this clinical phenomenon.
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Zhang et al. (2022) studied Pulmonary arterial hypertension. Bmpr2 ± mice model was evaluated on Suitability as a model for iron deficiency in pulmonary vascular disease. Bmpr2 ± transgenic mice are an inadequate model for studying iron deficiency in pulmonary vascular disease.
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