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Related Concept Videos

Heart Failure Drugs: Inhibitors of Renin-Angiotensin System01:26

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The activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system (RAAS) contributes to cardiac remodeling, and inhibiting the RAAS is a pharmacological target in heart failure management. As a result, neurohumoral modulation is a crucial treatment principle for managing heart failure. This approach involves using medications like ACE inhibitors (ACEIs), angiotensin receptor blockers (ARBs), β-blockers, mineralocorticoid receptor antagonists (MRAs), and neutral...
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Related Experiment Video

Updated: Mar 27, 2026

Suppression of Pro-fibrotic Signaling Potentiates Factor-mediated Reprogramming of Mouse Embryonic Fibroblasts into Induced Cardiomyocytes
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Ginsenoside Rb1 Mitigates Myocardial Fibrosis Through Inhibiting Exosomal-Derived miRNA-21-Associated Inflammation

Shihua Wang1, Weifeng Chi1, Yinghong Lu1

  • 1Department of Cardiology, Qingdao Hiser Hospital Affiliated of Qingdao University (Qingdao Traditional Chinese Medicine Hospital), Qingdao, China.

Cardiovascular Therapeutics
|March 26, 2026
PubMed
Summary

Ginsenoside Rb1 mitigates heart failure by reducing myocardial fibrosis and inflammation. It achieves this by downregulating exosomal miRNA-21 expression in mouse models, offering a potential therapeutic strategy.

Keywords:
angiotensin IIexosomeginsenoside Rb1miRNA-21myocardial fibrosis

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Area of Science:

  • Cardiovascular Biology
  • Molecular Medicine
  • Pharmacology

Background:

  • Myocardial fibrosis is a key factor in heart failure progression.
  • Natural compounds offer potential therapeutic avenues for heart failure management.
  • Ginsenoside Rb1 is investigated for its cardioprotective effects.

Purpose of the Study:

  • To investigate the antifibrotic and anti-inflammatory effects of Ginsenoside Rb1.
  • To elucidate the role of exosomal miRNA-21 in Ginsenoside Rb1's mechanism of action.
  • To evaluate Ginsenoside Rb1 in an Angiotensin II-induced mouse model of cardiac fibrosis.

Main Methods:

  • Primary mouse cardiac fibroblasts (pMCFs) and C57BL/6J mice were used for in vitro and in vivo studies.
  • Techniques included qPCR, Western blotting, NTA, BrdU staining, and ELISA.
  • Exosome characterization and analysis of fibrosis markers (COL1a1, COL3a1, ACTA2, TGFβ1) and miRNA-21 expression were performed.

Main Results:

  • Ginsenoside Rb1 prevented Angiotensin II-induced cell death and proliferation in pMCFs.
  • Rb1 inhibited Angiotensin II-induced expression of cardiac fibrosis markers in exosomes from pMCFs and mouse models.
  • Rb1 suppressed inflammatory responses and downregulated exosomal miRNA-21 expression in vivo.

Conclusions:

  • Ginsenoside Rb1 attenuates myocardial fibrosis and inflammation.
  • The mechanism involves the downregulation of exosomal miRNA-21.
  • Ginsenoside Rb1 shows promise as a therapeutic agent for heart failure.