THE SIGNIFICANCE OF ENDOTHELIAL DYSFUNCTION IN HEMORRHAGIC VASCULITIS
Article Sidebar
Main Article Content
Abstract
Immunoglobulin A (IgA) vasculitis (IgAV), also known as Henoch-Schönlein purpura, is the most common form of childhood vasculitis. It is characterized by cutaneous hemorrhage, resulting from red blood cell leakage into the skin or mucosae, possibly caused by damage to small blood vessels. These acute symptoms usually disappear without treatment. Endothelial cells are distributed on the inner surfaces of blood vessels and lymphatic vessels, and have important functions in metabolism and endocrine function, as well as being the primary targets of external stimuli and endogenous immune activity. Injury to endothelial cells is a feature of IgA vasculitis. Endothelial cell damage may be related to the deposition of immune complexes, the activation of complement, inflammatory factors, and chemokines, oxidative stress, hemodynamics, and coagulation factors. Both epigenetic mechanisms and genetic diversity provide a genetic background for endothelial cell injury. Here, research on the role of endothelial cells in allergic IgA vasculitis is reviewed.
Article Details
References
Aleyd E., van Hout M. W., Ganzevles S. H., Hoeben K. A., Everts V., Bakema J. E., et al. (2014). IgA enhances NETosis and release of neutrophil extracellular traps by polymorphonuclear cells via Fcalpha receptor I. J. Immunol. 192 2374–2383. 10.4049/jimmunol.1300261 [PubMed] [CrossRef] [Google Scholar]
Arneth B., Arneth R. (2021). Neutrophil Extracellular Traps (NETs) and Vasculitis. Int. J. Med. Sci. 18 1532–1540. 10.7150/ijms.53728 [PMC free article] [PubMed] [CrossRef] [Google Scholar]
Bian Y. F., Yang H. Y., Yang Z. M., Gao F., Zhang N. N., Xiao C. S. (2011). Amlodipine treatment prevents angiotensin II-induced human umbilical vein endothelial cell apoptosis. Arch. Med. Res. 42 22–27. 10.1016/j.arcmed.2011.01.012