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Impaired Lung BCAA Metabolism Promotes Ferroptosis and Resultant Pulmonary Arterial Hypertension-Associated Hepatopathy
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DOI：10.1016/j.jacbts.2026.101573.png)
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Abstract
En 中文
• Dysregulated lung BCAA metabolism contributes to PAH and multiorgan dysfunction. • Impaired BCAA catabolism promotes PASMC ferroptosis and pulmonary vascular remodeling. • Enhancing BCAA catabolism improves PAH severity, right ventricular function, and counteracts hepatic abnormalities. • Future studies could evaluate BCAA-targeted therapies as novel metabolic therapies in PAH patients.
Keywords:
branched-chain amino acids
ferroptosis
hepatopathy
pulmonary arterial hypertension
right ventricular failure
BCAA
branched-chain amino acid
MCT
monocrotaline
PAH
pulmonary arterial hypertension
PASMC
pulmonary artery smooth muscle cell
RVSP
right ventricular systolic pressure
SMC
smooth muscle cell
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