ReviewFrontiers in pharmacology2026
Mechanism of HIF-1α-mediated angiogenesis in rheumatoid arthritis and progress of natural medicine interventions.
Review in Frontiers in pharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by hyperplasia of synovial pannus and progressive joint destruction. Pathological angiogenesis, driven by hypoxia-inducible factor-1α (HIF-1α), constitutes a core pathological mechanism and has become a critical therapeutic target for RA. This article systematically elucidates the molecular mechanisms by which HIF-1α drives pathological angiogenesis through interactions with signaling pathways such as vascular endothelial growth factor (VEGF), angiogenin (ANG)-1/2, CXC chemokine ligand 12 (CXCL12)/CXC chemokine receptor 4 (CXCR4), phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt)/mammalian target of rapamycin (mTOR). HIF-1α-mediated angiogenesis forms a positive feedback network with pathological processes including synovial inflammatory response, glycolytic metabolic reprogramming, and oxidative stress-mitochondrial damage, collectively promoting synovial pannus formation. Additionally, this article summarizes the effects of traditional Chinese medicine formulations and plant-derived monomeric metabolites on HIF-1α-mediated RA synovial angiogenesis, as well as the preclinical research advances of anti-angiogenic mechanisms. It also briefly explores the potential of novel botanical drugs delivery systems in enhancing the targeting of natural products to the HIF-1α pathway and improving therapeutic efficacy, aiming to provide new perspectives and strategic options for HIF-1α-targeted RA therapies.
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