# Efficacy and safety of guanxinshutong capsule as adjunctive therapy for unstable angina: an integrated systematic review, meta-analysis, and network pharmacology study

**Authors:** Ya Li, Liyuan Yu, Lulu Wu, Weihang Peng, Qingmin Li, Peiying Huang, Xiaohui Chen, Ye Ye, Bojun Chen, Li Chen

PMC · DOI: 10.3389/fcvm.2026.1740334 · Frontiers in Cardiovascular Medicine · 2026-02-24

## TL;DR

This study shows that combining guanxinshutong capsule with standard treatment improves outcomes for unstable angina patients and identifies key biological pathways involved.

## Contribution

The study provides robust clinical evidence and pharmacological mechanisms for guanxinshutong capsule in treating unstable angina.

## Key findings

- Combining GXST with western medicine significantly improved clinical outcomes in unstable angina patients.
- Key signaling pathways involved are PI3K-Akt and MAPK, with compounds like kaempferol showing strong binding affinities.
- No significant differences were found in CK-MB, cTnI, or ARDI between treatment groups.

## Abstract

Unstable angina (UA), characterized by worsening chest pain and increased risk of acute myocardial infarction or sudden death, is a major clinical condition necessitating urgent and effective intervention. Although guanxinshutong capsule (GXST) has demonstrated preliminary therapeutic potential in alleviating angina symptoms, it lacks sufficient and robust clinical evidence to confirm its efficacy and safety in UA treatment. Therefore, further clinical research is urgently needed to validate the practical value of GXST in managing UA.

To determine the efficacy and safety of GXST as an adjunctive therapy for UA and to elucidate its potential pharmacological mechanisms.

Relevant RCTs were included to investigate the effectiveness of GXST in combination with WM for UA. ROB 2 was applied to assess their methodological quality. The data integration, evidence quality assessment, and trial sequence analysis were performed using R software, the GRADE framework, and TSA software, respectively. Concurrently, the network pharmacology was employed to identify disease-relevant targets, active components, and core targets of GXST. Crucially, bioinformatics analysis was conducted to explore the potential regulatory mechanisms.

Fifteen RCTs were included. Compared with WM monotherapy, GXST combined with WM exhibited significantly superior efficacy across multiple indicators: clinical effective rate(RR = 1.19, 95% CI = 1.13–1.25), ECG effective rate (RR = 1.20, 95% CI = 1.07–1.34), angina frequency (SMD = −2.20, 95% CI = −3.36 to −1.04), angina duration (SMD = −1.54, 95% CI = −2.14 to −0.94), PV levels(SMD = −0.82, 95% CI = −1.23 to −0.41), FIB levels(SMD = −1.18, 95% CI = −1.50 to −0.86), and TCM syndrome scores (SMD = −1.68, 95% CI = −2.18 to −1.18). However, no significant intergroup differences were detected in CK-MB, cTnI, or ARDI. KEGG enrichment analysis highlighted the PI3K-Akt and MAPK signaling pathways as central to the underlying mechanism. Molecular docking further demonstrated pronounced binding affinities of kaempferol, miltirone, and asiatic acid toward core targets AKT1, MAPK3, and PIK3CA, corroborating their therapeutic potential.

The combination therapy of GXST and WM significantly boosted clinical efficacy in patients with UA. Its mechanism of action involves regulating the PIK3CA/AKT1 and MAPK3 signaling pathways.

https://www.crd.york.ac.uk/PROSPERO/view/CRD42025634213, PROSPERO CRD42025634213.

Graphical abstract of the meta-analysis .Infographic summarizing a systematic review and meta-analysis on Guanxinshutong capsule (GXST) for unstable angina, showing data sources, 15 randomized controlled trials with 1,532 participants, improved clinical efficacy of GXST combined with western medicine, mechanisms, and diagram of a distressed patient with angina and plaque rupture.

Graphical abstract of the meta-analysis .

## Linked entities

- **Proteins:** AKT1 (AKT serine/threonine kinase 1), MAPK3 (mitogen-activated protein kinase 3), PIK3CA (phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha)
- **Chemicals:** kaempferol (PubChem CID 5280863), miltirone (PubChem CID 160142), asiatic acid (PubChem CID 119034)
- **Diseases:** unstable angina (MONDO:0006805)

## Full-text entities

- **Genes:** TNNI3 (troponin I3, cardiac type) [NCBI Gene 7137] {aka CMD1FF, CMD2A, CMH7, RCM1, TNNC1, cTnI}, AKT1 (AKT serine/threonine kinase 1) [NCBI Gene 207] {aka AKT, PKB, PKB-ALPHA, PRKBA, RAC, RAC-ALPHA}, PIK3CB (phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit beta) [NCBI Gene 5291] {aka P110BETA, PI3K, PI3KBETA, PIK3C1}, PIK3CA (phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) [NCBI Gene 5290] {aka CCM4, CLAPO, CLOVE, CWS5, HMH, MCAP}, MAPK3 (mitogen-activated protein kinase 3) [NCBI Gene 5595] {aka ERK-1, ERK1, ERT2, HS44KDAP, HUMKER1A, P44ERK1}
- **Diseases:** chest pain (MESH:D002637), angina (MESH:D000787), UA (MESH:D000789), acute myocardial infarction (MESH:D009203), sudden death (MESH:D003645)
- **Chemicals:** kaempferol (MESH:C006552), asiatic acid (MESH:C017032), miltirone (MESH:C068880), GXST (-)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

5 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12971700/full.md

## References

82 references — full list in the complete paper: https://tomesphere.com/paper/PMC12971700/full.md

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Source: https://tomesphere.com/paper/PMC12971700