ArticleNature neuroscience2012
The voltage-gated proton channel Hv1 enhances brain damage from ischemic stroke.
Article in Nature neuroscience, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 165 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
165 citing papers in PubMed, 254 citations in OpenAlex.
- Vitamin D alleviates intracerebral hemorrhage symptoms by modulating pro-inflammatory/anti-inflammatory phenotypic transformation of microglia through P2X7R activation of NLRP3.IBRO neuroscience reports · 2026Article
- Bdelloid rotifers harbor a voltage-gated proton channel with distinct mechanistic features.Nature communications · 2026Article
- Thermodynamic Frontiers in Hemoglobin-Inspired Polymer Science for Diagnosis and Modulation of Neurodegenerative Diseases.Cell biochemistry and function · 2026Review
- Amyloid precursor protein is a subunit of microglial Hv1 channels.Current opinion in immunology · 2026Review
- Voltage-gated proton channel Hv1/VSOP regulates reciprocal interactions between F-actin and endosomes in microglia.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Phagocytosis and neuroinflammation: orchestrating central nervous system homeostasis, repair, and the resolution of inflammation.Trends in neurosciences · 2026Review
- Microglial HVCN1 Deficiency Improves Movement and Survival of SOD1Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Stimuli-Responsive Biomimetic Nanomedicines for Targeted Therapy in Ischemic Stroke: Design Principles, Preclinical Evidence and Translational Challenges.International journal of nanomedicine · 2026Review
- Epigenetic and transcriptomic alterations precede amyloidosis in the Alzheimer's disease AppScientific reports · 2025Article
- Hv1 inhibition rescues AD pathology by restoring microglial mitochondrial function and enhancing mitochondrial transfer.Experimental & molecular medicine · 2025Article
- C6 peptide blockade of Hv1 channels inhibits neutrophil migration into the lungs to suppress Pseudomonas aeruginosa-induced acute lung injury.Respiratory research · 2025Article
- Amyloid precursor protein and C99 are subunits in human microglial Hv1 channels that enhance current and inflammatory mediator release.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Microglial voltage-gated proton channel 1 ablation in diabetic mice mitigates diabetes-driven demyelination and cognitive decline.World journal of psychiatry · 2025Article
- Hv1 channel in immune cells and pharmacology.Pharmacological research · 2025Review
- Brain targeted lipid nanoparticles with Hv1 inhibitors alleviate neuroinflammation post-ischemic stroke.Journal of nanobiotechnology · 2025Article
- Inhibition of the microglial voltage-gated proton channel 1 channel ameliorates diabetes-associated cognitive dysfunction by regulating axon demyelination.World journal of psychiatry · 2025Article
- Nanotechnology approaches to drug delivery for the treatment of ischemic stroke.Bioactive materials · 2025Review
- Fluctuating hydrogen-bond network of the Hv1 ion channel.Computational and structural biotechnology journal · 2025Article
- Validation of HvFrontiers in cellular neuroscience · 2025Article
- Dimerization is required for the glycosylation of S1-S2 linker of sea urchin voltage-gated proton channel Hv1.Biophysical journal · 2024Article
105 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
9 authors at 5 institutions in 1 country.
Funding
Abstract
Phagocytic cell NADPH oxidase (NOX) generates reactive oxygen species (ROS) as part of innate immunity. Unfortunately, ischemia can also induce this pathway and inflict damage on native cells. The voltage-gated proton channel Hv1 enables NOX function by compensating cellular loss of electrons with protons. Accordingly, we investigated whether NOX-mediated brain damage in stroke can be inhibited by suppression of Hv1. We found that mouse and human brain microglia, but not neurons or astrocytes, expressed large Hv1-mediated currents. Hv1 was required for NOX-dependent ROS generation in brain microglia in situ and in vivo. Mice lacking Hv1 were protected from NOX-mediated neuronal death and brain damage 24 h after stroke. These results indicate that Hv1-dependent ROS production is responsible for a substantial fraction of brain damage at early time points after ischemic stroke and provide a rationale for Hv1 as a therapeutic target for the treatment of ischemic stroke.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.