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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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Ginsenoside Rg1 Improves Cardiac Function and Ventricular Remodelling by Down-Regulating SH2B Adaptor Protein 1

Na Xiang1, Jiayun Hu1, Xueting Luo1,2

  • 1Department of Cardiology, Hubei Provincial Hospital of Traditional Chinese Medicine (Affiliated Hospital of Hubei University of Chinese Medicine), Wuhan, Hubei, China.

Clinical and Experimental Pharmacology & Physiology
|April 22, 2026
PubMed
Summary
This summary is machine-generated.

Ginsenoside Rg1 improves heart function after myocardial infarction by reducing SH2B1 protein levels. This natural compound offers a potential therapeutic strategy for acute myocardial infarction (AMI) and ventricular remodeling.

Keywords:
SH2 domain‐containing adapter protein B1cardiac functionginsenoside Rg1myocardial infarctionventricular remodelling

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Area of Science:

  • Cardiology
  • Pharmacology
  • Molecular Biology

Background:

  • Acute myocardial infarction (AMI) is a leading cause of global mortality.
  • Ginsenoside Rg1 (Rg1) is a compound with potential therapeutic properties.
  • SH2 domain-containing adapter protein B1 (SH2B1) plays a role in cardiac function.

Purpose of the Study:

  • To investigate the mechanism of Rg1 in ameliorating cardiac function and ventricular remodeling in AMI rats.
  • To explore the role of SH2B1 in mediating the cardioprotective effects of Rg1.
  • To determine if Rg1 regulates SH2B1 expression.

Main Methods:

  • Established an AMI rat model by ligating the left anterior descending coronary artery.
  • Conducted gain- and loss-of-function experiments for SH2B1.
  • Evaluated cardiac function and ventricular remodeling using echocardiography, ELISA, and histology.
  • Analyzed SH2B1 expression via RT-qPCR and Western blot; performed molecular docking.

Main Results:

  • Rg1 dose-dependently improved cardiac function, reduced inflammation, infarct size, apoptosis, and fibrosis in AMI rats.
  • SH2B1 expression was elevated in AMI rats, and Rg1 reduced it.
  • Molecular docking suggested Rg1 binds to SH2B1.
  • SH2B1 knockdown improved cardiac function; SH2B1 overexpression counteracted Rg1's benefits.

Conclusions:

  • Rg1 improves cardiac function and ventricular remodeling in AMI rats by down-regulating SH2B1.
  • The cardioprotective effects of Rg1 are partially mediated by the reduction of SH2B1.
  • Targeting SH2B1 may be a therapeutic strategy for AMI.