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.
Su et al. (Thu,) studied this question.