Beta-Alanine Supplementation Ameliorates Right Ventricular Remodeling Caused by Monocrotaline-Induced Pulmonary Hypertension
Hongling Su, Bo Li, Zhaoxia Guo, Fu Zhang, Aqian Wang, Kaiyu Jiang, Hai Zhu, Yanxia Yang, Jing Zeng, Wen Li, Yunshan Cao, Jian Liu
https://doi.org/10.1002/pul2.70244
Abstract
Pulmonary hypertension (PH) causes progressive pulmonary vascular resistance and right heart failure. We investigated whether beta-alanine (β-Ala) improves right ventricular (RV) remodeling and dysfunction in a monocrotaline (MCT)-induced PH rat model. Male Wistar rats were assigned to control, MCT-PH, and β-Ala-treated PH groups. RV function was assessed by RVSP and RVHI; molecular changes were examined by western blotting and qPCR; histology evaluated RV hypertrophy and fibrosis. β-Ala significantly improved RVSP and RVHI versus MCT. Mechanistically, β-Ala reduced ERK and p38 MAPK signaling while enhancing AKT activation. It decreased proapoptotic Bax and cleaved Caspase-3 and increased antiapoptotic Bcl-2. qPCR showed downregulation of ANP, BNP, β-MHC, and TGF-β, with upregulation of β-MHC. Histological analyses confirmed attenuation of RV hypertrophy and fibrosis. Overall, β-Ala mitigates RV remodeling and dysfunction in MCT-induced PH, likely via modulation of MAPK/AKT pathways and apoptosis, supporting its potential as a therapy for PH-related right heart dysfunction.
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