Lupus & antiphospholipid syndrome
Anti-endothelin receptor A autoantibodies associate with immunovascular risk and activate endothelial signalling in SLE
Authors' conclusion
Anti-ETAR autoantibodies associate with immunovascular risk and endothelial activation in SLE and directly stimulate endothelial signalling through a non-canonical ETAR-dependent mechanism.
Study context
- Population
- Women with SLE and non-SLE controls (pilot cohort) and an independent validation cohort stratified by SLE and hypertension (HTN) statuspilot and validation cohorts
- Exposure
- Women with SLE vs non-SLE controls, stratified by SLE and hypertension status
Methodological detailspilot cohort and independent validation cohort, multivariable models, mechanistic studies in primary human renal endothelial cells
- Pilot cohort and independent validation cohort
- Multivariable models
- Mechanistic studies in primary human renal endothelial cells
Main finding
As reported in the abstract
- Anti-ETAR and anti-ETBR autoantibodies elevated in SLE across both cohorts, highest in SLE with HTN
- Anti-ETAR showed the strongest association with sVCAM-1 and independently identified women with the highest endothelial activation burden beyond clinical covariates and anti-dsDNA
- In primary human renal endothelial cells (HRECs), SLE-derived IgG induced Ca2+ flux attenuated by ET receptor antagonism
- Blockade of the ETAR extracellular loop 2 domain reduced IgG-mediated Ca2+ signalling (non-canonical ETAR activation)
Observational data: associations, not effects.
Original publication
Anti-endothelin receptor A autoantibodies associate with immunovascular risk and activate endothelial signalling in SLE. Lupus Sci Med. Published 1 July 2026. doi:10.
Composed by AI from the published abstract and checked against it. How Briefs are made →