BMPR2型
脂毒性
内科学
内分泌学
突变体
医学
脂质代谢
CD36
生物
骨形态发生蛋白
生物化学
受体
基因
胰岛素抵抗
胰岛素
作者
Megha Talati,Evan L. Brittain,Joshua P. Fessel,Niki Penner,James R. Atkinson,Mitch Funke,Carrie A. Grueter,W. Gray Jerome,Michael L. Freeman,John H. Newman,James West,Anna R. Hemnes
标识
DOI:10.1164/rccm.201507-1444oc
摘要
Taken together, our data suggest that impaired FAO and increased expression of the lipid transporter CD36 are key mechanisms underlying lipid deposition in the BMPR2-mutant RV, which are exacerbated in the presence of dietary lipids. These findings suggest important features leading to RV lipotoxicity in pulmonary arterial hypertension and may point to novel areas of therapeutic intervention.
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