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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: May 11, 2025

Manufacturing Abdominal Aorta Hydrogel Tissue-Mimicking Phantoms for Ultrasound Elastography Validation
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RAGE deficiency ameliorates abdominal aortic aneurysm progression.

Cong Bi1, Bingqi Liu1, Peixian Gao1

  • 1Department of Vascular Surgery, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, 250021, Shandong, China.

Inflammation Research : Official Journal of the European Histamine Research Society ... [Et Al.]
|April 17, 2025
PubMed
Summary

Receptor for advanced glycation end products (RAGE) deficiency reduces abdominal aortic aneurysm (AAA) progression by decreasing inflammation and altering macrophage polarization. This suggests RAGE is a potential therapeutic target for AAA.

Keywords:
Abdominal aortic aneurysmsInflammationMacrophage polarizationReceptor for advanced glycation end products

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Area of Science:

  • Vascular Biology
  • Immunology
  • Molecular Medicine

Background:

  • Abdominal aortic aneurysm (AAA) involves inflammation and arterial wall degradation.
  • The receptor for advanced glycation end products (RAGE) influences inflammatory pathways, but its role in AAA is not fully understood.

Purpose of the Study:

  • To investigate RAGE's role in AAA pathogenesis.
  • To examine RAGE expression in human and mouse AAA tissues.
  • To determine the effects of RAGE deficiency on AAA progression, macrophage polarization, and inflammation.

Main Methods:

  • Analyzed RAGE expression in human AAA and mouse models (porcine pancreatic elastase-induced).
  • Utilized Western blotting, immunohistochemistry, and immunofluorescence.
  • Assessed AAA progression in RAGE-deficient mice and studied macrophage polarization and NF-κB signaling in vitro.

Main Results:

  • Elevated RAGE expression observed in AAA tissues, especially in macrophages.
  • RAGE deficiency reduced AAA incidence, mortality, and aortic dilation.
  • Preserved aortic structure, decreased inflammatory infiltration, and suppressed M1 macrophage polarization and pro-inflammatory cytokines via NF-κB pathway.

Conclusions:

  • RAGE deficiency mitigates AAA progression by modulating macrophage polarization and reducing inflammation through the NF-κB pathway.
  • RAGE emerges as a potential therapeutic target for abdominal aortic aneurysm.