Pyridoxamine Attenuates PAH by Inhibiting the Receptor for Advanced Glycation end Products in Macrophages

Right Heart Journal 2026 Open access

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Authors: Kuk Hui Son, Seyeon Oh, Albert Youngwoo Jang, Kyunghee Byun, Wook-Jin Chung
DOI: 10.65721/rhj.2026.1.e5
Cited by: 2
References: 50

Abstract

Background: The receptor for advanced glycation end products (RAGEs) and macrophage activation are involved in the pathophysiology of pulmonary artery hypertension (PAH).We hypothesized that activated macrophages could aggravate PAH through the inflammatory RAGE pathway and that pyridoxamine (PM) could attenuate PAH in monocrotaline-and Sugen 5416/hypoxia (SuHx)-induced PAH animal models.Methods: We evaluated the effect of PM on macrophage activation, inflammatory cytokine expression (interleukin [IL]-1β, IL-6, and tumor necrosis factor-α), RAGE and RAGE ligands (advanced glycation end products [AGEs], high motility group box 1 protein, and S100 calcium-

Fields of Study & Subjects

Advanced Glycation End Products research Immune cells in cancer Peroxisome Proliferator-Activated Receptors

Publication details

Journal / source
Right Heart Journal
Publisher
XMLink
Volume
1
Issue
1
Publication date
1 January 2026
Language
EN