ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025
Artesunate Inhibits Neointimal Hyperplasia by Promoting IRF4 Associated Macrophage Polarization.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Artemisinin and its derivatives for metabolic syndrome: From multi‑target mechanisms to translational opportunities (Review).Molecular medicine reports · 2026Review
- Neointimal hyperplasia and vascular restenosis: from molecular mechanisms to therapeutic interventions.Molecular biomedicine · 2026Review
- Modulation and Reprogramming of Adipose Tissue Macrophages in Obesity.Biomolecules · 2026Review
- Artesunate nanoliposomes in hepatocellular carcinoma: mechanistic ferroptosis induction and translational opportunities.Discover oncology · 2026Review
- Therapeutic targeting of myeloid cells in liver fibrosis: Mechanisms and clinical prospects.Animal models and experimental medicine · 2025Review
- Artesunate Inhibits Neointimal Hyperplasia by Promoting IRF4 Associated Macrophage Polarization.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- From malaria fighter to diabetes guardian: the emerging role of artesunate in treating diabetes and diabetic complications.Frontiers in pharmacology · 2025Review
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Authors and funding
16 authors.
Funding
Abstract
Vascular restenosis is a serious clinical issue initiated and aggravated by macrophage inflammation, with no effective treatments available, in cardiovascular and autoimmune diseases. However, the untapped mechanisms and new targets that can regulate macrophage polarization and vascular restenosis remain elusive. The research identifies interferon regulatory factor 4 (IRF4) expression as crucial in macrophage polarization during arterial restenosis. Myeloid-specific Irf4 deficiency and overexpression experiments showed that IRF4 promoted M2 macrophage polarization, inhibited M1 macrophage transitions, and disrupted the interaction between macrophages and vascular smooth muscle cells to reduce neointimal hyperplasia by directly upregulating krüppel like factor 4 (KLF4) expression. Artesunate, an FDA-approved drug, is screened as a potent activator of IRF4 expression in M2 polarization, and its treatment attenuated arterial restenosis in rodents and non-human primates. The findings reveal a significant protective role of IRF4 in the development of neointimal hyperplasia by regulating macrophage polarization, and artesunate may be proposed as a novel therapy for vascular restenosis.
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