Evidence map›Paper›PMID 33897377›Full record

ReviewFrontiers in cellular neuroscience2021

Functions and Mechanisms of the Voltage-Gated Proton Channel Hv1 in Brain and Spinal Cord Injury.

Junyun He, Rodney M Ritzel, Junfang Wu

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in cellular neuroscience, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.2field-weighted citation impact, top 12% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

16 citing papers in PubMed, 33 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Article
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  7. Article
  8. Review
  9. Deletion of Slc9a1 in Cx3cr1Journal of neuroinflammation · 2024
    Article
  10. Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. NADPH Oxidases in Pain Processing.Antioxidants (Basel, Switzerland) · 2022
    Review
  16. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Junyun HeDepartment of Anesthesiology and Center for Shock, Trauma and Anesthesiology Research (STAR), University of Maryland School of Medicine, Baltimore, MD, United States.
Rodney M RitzelDepartment of Anesthesiology and Center for Shock, Trauma and Anesthesiology Research (STAR), University of Maryland School of Medicine, Baltimore, MD, United States.
Junfang WuDepartment of Anesthesiology and Center for Shock, Trauma and Anesthesiology Research (STAR), University of Maryland School of Medicine, Baltimore, MD, United States.
University of Maryland, Baltimore · US

Funding

The new roles of the autophagy-lysosomal pathway in spinal cord injury-mediated dementiaR01NS094527 · NINDS · UNIVERSITY OF MARYLAND BALTIMORE · PI MARTA M LIPINSKI, Junfang Wu · 2016 to 2026
$3.5M
Dementia Following Spinal Cord Injury: Mechanism and Therapeutic TargetingRF1NS110637 · NINDS · UNIVERSITY OF MARYLAND BALTIMORE · PI JAY, STEVEN MICHAEL, WU, JUNFANG · 2019 to 2019
$2.8M
Mechanism of Inflammatory Related Brain Dysfunction after Spinal Cord InjuryR01NS110635 · NINDS · UNIVERSITY OF MARYLAND BALTIMORE · PI FADEN, ALAN IRA, WU, JUNFANG · 2019 to 2023
$2.2M
The Function and Mechanisms of Voltage-Gated Proton Channel Hv1 in Spinal Cord InjuryR01NS110825 · NINDS · UNIVERSITY OF MARYLAND BALTIMORE · PI WU, JUNFANG · 2020 to 2024
$1.9M
NINDS NIH HHS R01 NS094527NINDS NIH HHS R01 NS110635NINDS NIH HHS R01 NS110825NINDS NIH HHS RF1 NS110637
6 · The paper itself

Abstract

The voltage-gated proton channel Hv1 is a newly discovered ion channel that is highly conserved among species. It is known that Hv1 is not only expressed in peripheral immune cells but also one of the major ion channels expressed in tissue-resident microglia of the central nervous systems (CNS). One key role for Hv1 is its interaction with NADPH oxidase 2 (NOX2) to regulate reactive oxygen species (ROS) and cytosolic pH. Emerging data suggest that excessive ROS production increases and requires proton currents through Hv1 in the injured CNS, and manipulations that ablate Hv1 expression or induce loss of function may provide neuroprotection in CNS injury models including stroke, traumatic brain injury, and spinal cord injury. Recent data demonstrating microglial Hv1-mediated signaling in the pathophysiology of the CNS injury further supports the idea that Hv1 channel may function as a key mechanism in posttraumatic neuroinflammation and neurodegeneration. In this review, we summarize the main findings of Hv1, including its expression pattern, cellular mechanism, role in aging, and animal models of CNS injury and disease pathology. We also discuss the potential of Hv1 as a therapeutic target for CNS injury.

Indexed as

acidificationmicrogliaNOX2ROSspinal cord injurystroketraumatic brain injuryvoltage-gated proton channel Hv1

Identifiers

PMID33897377
PMCPMC8063047
OpenAlexW3156204327

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.