Key result
Impaired fatty acid oxidation and CD36 drive lipid deposition in BMPR2-mutant RVs, exacerbated by high-lipid diets.
Impaired fatty acid oxidation and increased CD36 expression are key mechanisms of right ventricular lipotoxicity in BMPR2-mutant pulmonary arterial hypertension.
Suggests dietary lipid restriction as a potential RV-protective strategy in BMPR2-mutant PAH; leaves open human translation of CD36-targeted therapies.
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Talati et al. (2016) studied Pulmonary arterial hypertension. BMPR2 mutation and Western diet vs. Wild-type controls and standard diet was evaluated on Lipid accumulation and fatty acid oxidation. Impaired fatty acid oxidation and increased expression of the lipid transporter CD36 drive lipid deposition in the BMPR2-mutant right ventricle, which is further exacerbated by a high-lipid diet.
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