Evidence map›Paper›PMID 42415687›Full record

ArticleCardiovascular therapeutics2026

Salvianolic Acid B Alleviates Atrial Fibrillation-Associated Fibrosis With Modulation of COL1A2 and the PI3K-AKT Pathway.

Pengran Wang, Jianhua Ma, Jianlong Li, Shanshan Li, Yeran Zhu, Ruibin Li, Jidong Zhang

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cardiovascular therapeutics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

The trial behind it

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Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors.

Pengran WangDepartment of Cardiology, The Second Hospital of Hebei Medical University, Shijiazhuang, Hebei, China, hebmu.edu.cn.ORCID https://orcid.org/0009-0005-3827-1759
Jianhua MaEmergency Department, Affiliated Hospital of Hebei University, Baoding, Hebei, China, hbu.cn.ORCID https://orcid.org/0009-0002-9429-2800
Jianlong LiDepartment of Cardiology, Affiliated Hospital of Hebei University, Baoding, Hebei, China, hbu.cn.ORCID https://orcid.org/0009-0004-8818-1965
Shanshan LiDepartment of Cardiology, The Second Hospital of Hebei Medical University, Shijiazhuang, Hebei, China, hebmu.edu.cn.ORCID https://orcid.org/0009-0009-5335-8966
Yeran ZhuDepartment of Cardiology, Affiliated Hospital of Hebei University, Baoding, Hebei, China, hbu.cn.ORCID https://orcid.org/0009-0008-4039-1014
Ruibin LiDepartment of Cardiology, The Second Hospital of Hebei Medical University, Shijiazhuang, Hebei, China, hebmu.edu.cn.ORCID https://orcid.org/0000-0002-0807-662X
Jidong ZhangDepartment of Cardiology, The Second Hospital of Hebei Medical University, Shijiazhuang, Hebei, China, hebmu.edu.cn.ORCID https://orcid.org/0009-0003-0100-8290

Funding

Medical Science Research Project of Hebei GZ2023011
6 · The paper itself

Abstract

backgroundAtrial 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.

methodsTranscriptome 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-CaCl

resultsCOL1A2 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

conclusionsSal-B alleviates AF in association with COL1A2 modulation and PI3K-AKT signaling pathway inhibition, which may contribute to reducing atrial fibrosis.

Indexed as

Anti-Arrhythmia AgentsAntifibrotic AgentsAtrial FibrillationAtrial RemodelingBenzofuransCollagen Type IMyocytes, CardiacPhosphatidylinositol 3-KinaseProto-Oncogene Proteins c-aktAnimalsApoptosisCell LineCell MovementDepsidesDisease Models, AnimalFibrosisAnti-Arrhythmia AgentsAntifibrotic AgentsBenzofuransCollagen Type ICollagen Type I, alpha2 SubunitDepsidesPhosphatidylinositol 3-KinaseProto-Oncogene Proteins c-aktsalvianolic acid Batrial fibrillationatrial fibrosisCOL1A2PI3K-AKT pathwaysalvianolic acid B

Identifiers

PMID42415687
PMCPMC13598933

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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 OpenQuestion graph.