# Exploring Astragaloside IV in Ischemic Heart Disease: A Comprehensive Systematic Review and Meta‐Analysis of Preclinical Cardiotoxicity Models

**Authors:** Alosh Greeny, Gollapalle Lakshminarayanashastry Viswanatha, Rekha Raghuveer Shenoy, Shylaja Hanumanthappa, Dinesh Kumar Chellappan, Jagnoor Singh Sandhu, Saumya Khanna, Nandakumar Krishnadas

PMC · DOI: 10.1002/jbt.70365 · 2025-06-23

## TL;DR

This study reviews preclinical evidence showing Astragaloside IV reduces heart damage and improves function in ischemic heart disease through multiple mechanisms.

## Contribution

A comprehensive meta-analysis of 18 preclinical studies on Astragaloside IV's cardioprotective effects in ischemic heart disease.

## Key findings

- As-IV significantly reduces myocardial infarction size and apoptosis in ischemic heart disease models.
- As-IV improves cardiac function by increasing ejection fraction and reducing left ventricular dimensions.
- As-IV exhibits anti-inflammatory and pro-angiogenic effects through modulation of key biomarkers.

## Abstract

This systematic review and meta‐analysis were conducted to evaluate the therapeutic efficacy of Astragaloside IV (As‐IV) in ischemic heart disease based on the preclinical evidence and to correlate the cardioprotective effect with various available mechanisms. This systematic review and meta‐analysis were conducted based on the results of a thorough literature search in databases of published papers, such as PubMed, Embase, and Google Scholar. A total of 18 studies that met the inclusion/exclusion criteria were included. The meta‐analysis has shown the significant therapeutic efficacy of As‐IV on ischemic heart disease. As‐IV has decreased the myocardial infarction size, the left ventricular weight indices, the left ventricular internal diameter in systole, and the left ventricular internal diameter in diastole. As‐IV has decreased the level of the third type of collagen and the decreased activity of creatine kinase and lactate dehydrogenase. Also, As‐IV has markedly decreased the rate of apoptosis and the expression of the proapoptotic markers such as caspase‐3 and Bax. The left ventricular systolic pressure, as well as the arterial shortening edge and the ejection fraction, has increased. The levels of the antiapoptotic protein Bcl‐2 increased. In addition, As‐IV has a powerful anti‐inflammatory influence by inhibiting the main markers of inflammation, such as TLR4, IL‐1, TNF‐α, and TGF‐β. As‐IV has also caused an effect on angiogenesis by increasing the VEGF level. The results have revealed the As‐IV, as a decent universal medicine for ischemic heart disease because of its variety of actions and effectiveness.

This systematic review and meta‐analysis evaluated the therapeutic efficacy of Astragaloside IV in ischemic heart disease, encompassing 18 preclinical studies. The findings demonstrated that As‐IV significantly reduced myocardial infarction size and apoptosis while improving cardiac function and angiogenesis through various mechanisms, along with potent anti‐oxidant, anti‐apoptotic, and anti‐inflammatory effects. These results suggest that As‐IV is a promising universal treatment for ischemic heart disease.

## Linked entities

- **Proteins:** Casp3 (caspase 3), BAX (BCL2 associated X, apoptosis regulator), BCL2 (BCL2 apoptosis regulator), VEGFA (vascular endothelial growth factor A), TLR4 (toll like receptor 4), IL1A (interleukin 1 alpha), TNF (tumor necrosis factor), TGFB1 (transforming growth factor beta 1)
- **Chemicals:** Astragaloside IV (PubChem CID 158694)
- **Diseases:** ischemic heart disease (MONDO:0024644)

## Full-text entities

- **Genes:** TNF (tumor necrosis factor) [NCBI Gene 7124] {aka DIF, IMD127, TNF-alpha, TNFA, TNFSF2, TNLG1F}, IL1A (interleukin 1 alpha) [NCBI Gene 3552] {aka IL-1 alpha, IL-1A, IL1, IL1-ALPHA, IL1F1}, BAX (BCL2 associated X, apoptosis regulator) [NCBI Gene 581] {aka BCL2L4}, VEGFA (vascular endothelial growth factor A) [NCBI Gene 7422] {aka L-VEGF, MVCD1, VEGF, VPF}, TLR4 (toll like receptor 4) [NCBI Gene 7099] {aka ARMD10, CD284, TLR-4, TOLL}, BCL2 (BCL2 apoptosis regulator) [NCBI Gene 596] {aka Bcl-2, PPP1R50}, CASP3 (caspase 3) [NCBI Gene 836] {aka CPP32, CPP32B, SCA-1}
- **Diseases:** Ischemic Heart Disease (MESH:D017202), inflammation (MESH:D007249), Cardiotoxicity (MESH:D066126), myocardial infarction (MESH:D009203)
- **Chemicals:** As-IV (MESH:C052064)

## Figures

12 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12186012/full.md

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Source: https://tomesphere.com/paper/PMC12186012