Salvianolic Acid B Alleviates Atrial Fibrillation-Associated Fibrosis With Modulation of COL1A2 and the PI3K-AKT Pathway.
P, W., J, M., J, L., S, L., Y, Z., R, L., & J, Z. (2026). Salvianolic Acid B Alleviates Atrial Fibrillation-Associated Fibrosis With Modulation of COL1A2 and the PI3K-AKT Pathway.. Cardiovascular therapeutics. https://doi.org/10.1155/cdr/5515602
P W, J M, J L, S L, Y Z, R L, et al. Salvianolic Acid B Alleviates Atrial Fibrillation-Associated Fibrosis With Modulation of COL1A2 and the PI3K-AKT Pathway.. Cardiovascular therapeutics. 2026; doi: 10.1155/cdr/5515602
P W, J M, J L, et al. Salvianolic Acid B Alleviates Atrial Fibrillation-Associated Fibrosis With Modulation of COL1A2 and the PI3K-AKT Pathway.[J]. Cardiovascular therapeutics. 2026. DOI: 10.1155/cdr/5515602.
@article{p2026,
author = {Wang P and Ma J and Li J and Li S and Zhu Y and Li R and Zhang J},
title = {Salvianolic Acid B Alleviates Atrial Fibrillation-Associated Fibrosis With Modulation of COL1A2 and the PI3K-AKT Pathway.},
journal = {Cardiovascular therapeutics},
year = {2026},
doi = {10.1155/cdr/5515602},
note = {PMID: 42415687},
}
TY - JOUR AU - Wang P AU - Ma J AU - Li J AU - Li S AU - Zhu Y AU - Li R AU - Zhang J TI - Salvianolic Acid B Alleviates Atrial Fibrillation-Associated Fibrosis With Modulation of COL1A2 and the PI3K-AKT Pathway. T2 - Cardiovascular therapeutics PY - 2026 DO - 10.1155/cdr/5515602 AN - PMID:42415687 ER -
BACKGROUND: Atrial fibrillation (AF), the most prevalent cardiac arrhythmia, is strongly associated with atrial fibrosis. Salvianolic acid B (Sal-B), a bioactive compound extracted from Salvia miltiorrhiza, demonstrates cardioprotective properties, though its specific role in AF remains to be elucidated. METHODS: Transcriptome analysis of the GSE115574 dataset was performed to identify COL1A2 as a differentially expressed gene in patients with AF. Molecular docking simulations were performed to evaluate the binding affinity between Sal-B and COL1A2. For in vitro experiments, an injury model was established in AC16 cardiomyocytes using Angiotensin II (Ang-II) treatment, followed by intervention with either Sal-B (80 μg/mL) or COL1A2 siRNA. Cellular viability, apoptosis, migration capacity, and fibrosis markers (COL1A1, α-SMA, and collagen III) were subsequently assessed. In vivo studies employed an ACh-CaCl2-induced AF rat model, with cardiac function evaluated through electrocardiography (ECG) and echocardiography. Myocardial tissue damage was examined via hematoxylin-eosin (HE) staining and Masson's trichrome staining. Western blot analysis was used to determine COL1A2 expression and PI3K-AKT pathway activity. RESULTS: COL1A2 expression was significantly upregulated in AF, and molecular docking demonstrated its strong binding affinity for Sal-B. Sal-B treatment rescued Ang-II-induced cardiomyocyte damage, reduced apoptosis, and suppressed fibrosis marker expression. In rat models, either Sal-B or si-COL1A2 alone shortened the AF duration, improved cardiac function (attenuated the elevated E/E' ratio while restoring the ejection fraction), and reduced fibrosis and inflammation. The combined treatment synergistically restored sinus rhythm and normalized collagen deposition, suggesting a modulatory role of Sal-B in these processes. CONCLUSIONS: Sal-B alleviates AF in association with COL1A2 modulation and PI3K-AKT signaling pathway inhibition, which may contribute to reducing atrial fibrosis.