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January 9, 2026Korean Journal of Physiology and PharmacologyOpen Access

Astragaloside IV inhibits MAPK pathway and promotes mitochondrial autophagy in rats with heart failure

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Key result

AS-IV alleviates pressure overload-induced heart failure by improving mitochondrial function and activating mitophagy, possibly via inhibition of the MAPK pathway.

Authors

YWYaoyao WangYCYue ChenTLTengxian Li

Discussion

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Overview

Animal model reveals that Astragaloside IV improves mitochondrial function in heart failure, suggesting therapeutic potential.

Key Points

  • The aim is to explore the effects of Astragaloside IV on mitochondrial homeostasis in a rat model of heart failure.
  • Induced heart failure in rats using abdominal aortic constriction.
  • Administered Astragaloside IV at doses of 20 mg/kg and 80 mg/kg.
  • Measured parameters such as myocardial fibrosis, mitochondrial function, and MAPK pathway activation.
  • AS-IV treatment reduced myocardial fibrosis and hypertrophy.
  • Increased ATP and manganese superoxide dismutase levels were observed.
  • AS-IV enhanced mitochondrial autophagy and reduced reactive oxygen species.
  • Significant inhibition of the p38 MAPK pathway was noted.

Study Design

Type

RCT (n=24)

Blinding

null

Randomization

null

Multicenter

No

PICO

P
Population
Heart Failure (n=24)
I
Intervention / Comparator
Astragaloside IV vs 0.5% CMC vehicle (20 mg/kg and 80 mg/kg)
O
Primary Outcome
Myocardial fibrosis and hypertrophy — null (null), p=<0.001

Main Result

Effect estimate: null (95% CI null)

p-value: p=<0.001

Limitations

  • Direct molecular interactions were not verified.
  • Only one model of heart failure was used; additional validation in ischemic or diabetic cardiomyopathy models would enhance translational relevance.
  • Long-term safety, pharmacokinetics, and clinical efficacy remain to be investigated.

Cite This Study

Wang et al. (2025) conducted an RCT in Heart Failure (n=24). Astragaloside IV vs. 0.5% CMC vehicle was evaluated on Myocardial fibrosis and hypertrophy (null, 95% CI null, p=<0.001). AS-IV alleviates pressure overload-induced heart failure by improving mitochondrial function and activating mitophagy, possibly via inhibition of the MAPK pathway.

synapsesocial.com/papers/69612fe730ef6c21f6853f84https://doi.org/10.4196/kjpp.25.113
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Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1Astragaloside IV attenuates uremia-induced myocardial injury by inhibiting autophagy via ATF42025
  2. 2The interventional effect of astragaloside IV on rodent models of myocardial fibrosis: a systematic review and meta-analysis2025
  3. 3Astragaloside IV attenuates uremia-induced myocardial injury by inhibiting autophagy via ATF42025
  4. 4Astragaloside IV Binds with RhoA, Inhibits EndMT and Ameliorates Myocardial Fibrosis in Mice2025
  5. 5Astragaloside IV Ameliorates Cerebral Ischemic-Reperfusion Injury via Improving Mitochondrial Function and Inhibiting Neuronal Apoptosis2025