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
