Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2022 Mar 16:13:833954.
doi: 10.3389/fphys.2022.833954. eCollection 2022.

A Review of the Mechanism of Vascular Endothelial Injury in Immunoglobulin A Vasculitis

Shanshan Xu  1 , Shanshan Han  1 , Yanlin Dai  1 , Long Wang  1 , Xia Zhang  2 , Ying Ding  1
Affiliations
Review

A Review of the Mechanism of Vascular Endothelial Injury in Immunoglobulin A Vasculitis

Shanshan Xu et al. Front Physiol. .

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.

Keywords: gene polymorphisms; immunoglobulin A vasculitis; metabolomics markers; system of complement; vascular endothelial injury.

PubMed Disclaimer

Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Figures

FIGURE 1
FIGURE 1
Diagram of Gd-IgA1-containing complex in relation to endothelial cell injury in IgAV.
FIGURE 2
FIGURE 2
Diagram of IgAV endothelial injury mechanism.
See this image and copyright information in PMC

Similar articles

See all similar articles

Cited by

See all "Cited by" articles

References

    1. 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 - DOI - PubMed
    1. Arneth B., Arneth R. (2021). Neutrophil Extracellular Traps (NETs) and Vasculitis. Int. J. Med. Sci. 18 1532–1540. 10.7150/ijms.53728 - DOI - PMC - PubMed
    1. 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 - DOI - PubMed
    1. Brasier A. R. (2010). The nuclear factor-kappaB-interleukin-6 signalling pathway mediating vascular inflammation. Cardiovasc. Res. 86 211–218. 10.1093/cvr/cvq076 - DOI - PMC - PubMed
    1. Buscatti I. M., Casella B. B., Aikawa N. E., Watanabe A., Farhat S. C. L., Campos L. M. A., et al. (2018). Henoch-Schönlein purpura nephritis: initial risk factors and outcomes in a Latin American tertiary center. Clin. Rheumatol. 37 1319–1324. 10.1007/s10067-017-3972-3 - DOI - PubMed