ArticlePulmonary circulation2026
Beta-Alanine Supplementation Ameliorates Right Ventricular Remodeling Caused by Monocrotaline-Induced Pulmonary Hypertension.
Article in Pulmonary circulation, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors.
Funding
No grant is acknowledged in the PubMed record.
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.
Indexed as
Identifiers
What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.