ArticleFrontiers in cellular neuroscience2025
Endothelin-1 triggers oxidative stress and cytokine release in human microglia cells through ETRB-dependent mechanisms.
Article in Frontiers in cellular neuroscience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Resting Cytosolic and Nuclear Reactive Oxygen Species (ROS) Are Regulated by the Basal Activity of ET-1 Receptors in Human Vascular Smooth Muscle Cells.International journal of molecular sciences · 2026Article
- Article
- HMC3 revealed: how much do these "Microglia" really tell us?Frontiers in immunology · 2026Review
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7 authors.
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Abstract
Microglial cells are highly specialized cells of the central nervous system (CNS) that play dual roles in neuroprotection, but can also promote inflammation and neurodegeneration. Endothelin-1 (ET-1) is a potent vasoconstrictor that induces severe and prolonged cerebral vasoconstriction and inflammation. However, the mechanism of how ET-1 activates a proinflammatory response in the CNS is unknown. In this study, we demonstrate that ET-1 activates proinflammatory and oxidative stress responses in human HMC3 microglial cells via endothelin receptor B (ETRB). ET-1 treatment significantly increased nitric oxide (NO) and reactive oxygen species (ROS) production, and upregulated inducible nitric oxide synthase (iNOS) mRNA. These effects were attenuated by the selective ETRB antagonist BQ788, but not by the ETRA antagonist BQ123, suggesting a receptor-specific mechanism. ET-1 increases TNFα levels by 56% (
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