Evidence map›Paper›PMID 32624183›Full record

ArticleBritish journal of anaesthesia2020

Blocking Kv1.3 potassium channels prevents postoperative neuroinflammation and cognitive decline without impairing wound healing in mice.

Ieng K Lai, Martin Valdearcos, Kazuhito Morioka, Sarah Saxena, Xiaomei Feng, Rong Li, Yosuke Uchida, An Lijun, Wei Li, Jonathan Pan and 4 more

Erratum issuedOpen access · greenAbstract read
In one paragraph

Article in British journal of anaesthesia, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
3.1field-weighted citation impact, top 7% 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

15 citing papers in PubMed, 37 citations in OpenAlex.

  1. Review
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  6. Functional Potassium Channels in Macrophages.The Journal of membrane biology · 2023
    Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

14 authors at 2 institutions in 4 countries.

Ieng K LaiCenter for Cerebrovascular Research, Department of Anesthesia and Perioperative Care, University of California, San Francisco, CA, USA.
Martin ValdearcosDiabetes Center and Department of Medicine, University of California, San Francisco, CA, USA.
Kazuhito MoriokaOrthopaedic Trauma Institute, Department of Orthopaedic Surgery, University of California, San Francisco, CA, USA.
Sarah SaxenaCenter for Cerebrovascular Research, Department of Anesthesia and Perioperative Care, University of California, San Francisco, CA, USA; Department of Anesthesia, University Hospital Center CHU-Charleroi, Charleroi, Belgium.
Xiaomei FengCenter for Cerebrovascular Research, Department of Anesthesia and Perioperative Care, University of California, San Francisco, CA, USA; Department of Anesthesiology, University of Utah, Salt Lake City, UT, USA.
Rong LiCenter for Cerebrovascular Research, Department of Anesthesia and Perioperative Care, University of California, San Francisco, CA, USA; Department of Anesthesiology, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China.
Yosuke UchidaCenter for Cerebrovascular Research, Department of Anesthesia and Perioperative Care, University of California, San Francisco, CA, USA; Department of Anesthesiology and Critical Care Medicine, Hokkaido University Graduate School of Medicine, Sapporo, Japan.
An LijunWeill Institute for Neurosciences, Brain and Spinal Injury Center (BASIC), Department of Neurological Surgery, University of California, San Francisco, CA, USA; Department of Anesthesiology, The Affiliated Huaian No.1 People's Hospital of Nanjing Medical University, Huaian, China.
Wei LiWeill Institute for Neurosciences, Brain and Spinal Injury Center (BASIC), Department of Neurological Surgery, University of California, San Francisco, CA, USA; Department of Anesthesia, Shandong Provincial Hospital, Jinan, China.
Jonathan PanWeill Institute for Neurosciences, Brain and Spinal Injury Center (BASIC), Department of Neurological Surgery, University of California, San Francisco, CA, USA.
Suneil KoliwadDiabetes Center and Department of Medicine, University of California, San Francisco, CA, USA.
Ralph MarcucioOrthopaedic Trauma Institute, Department of Orthopaedic Surgery, University of California, San Francisco, CA, USA.
Heike WulffDepartment of Pharmacology University of California, Davis, CA, USA.
Mervyn MazeCenter for Cerebrovascular Research, Department of Anesthesia and Perioperative Care, University of California, San Francisco, CA, USA. Electronic address: Mervyn.Maze@UCSF.edu.
University of California, San Francisco · USUniversity of California, Davis · US

Funding

Research BaseP30DK063720 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI VAISSE, CHRISTIAN · 2003 to 2019
$21.8M
UCSF Nutrition Obesity Research CenterP30DK098722 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI CHRISTIAN VAISSE · 2015 to 2026
$14.6M
Microglia: dietary fat-sensitive mediators of inflammation and metabolic diseaseR01DK103175 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI KOLIWAD, SUNEIL KRISHNA · 2015 to 2019
$1.8M
Microglial K+ Channels in Ischemic StrokeR01NS100294 · NINDS · UNIVERSITY OF CALIFORNIA AT DAVIS · PI WULFF, HEIKE · 2017 to 2020
$1.3M
Inflammation resolving mechanism dysregulation in postoperative cognitive declineR01GM104194 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI MAZE, MERVYN · 2013 to 2016
$1.2M
Effects of Aging on Macrophages and Bone RegenerationR01AG046282 · NIA · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI MARCUCIO, RALPH S, NAKAMURA, MARY C · 2013 to 2016
$784k
Microglia: Diet-Sensitive Mediators Between Immunity and Hypothalamic FunctionK01DK113064 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI VALDEARCOS, MARTIN · 2018 to 2020
$461k
NIA NIH HHS R01 AG046282NIDDK NIH HHS K01 DK113064NIDDK NIH HHS P30 DK063720NIDDK NIH HHS R01 DK103175NIGMS NIH HHS R01 GM104194NINDS NIH HHS R01 NS100294
6 · The paper itself

Abstract

backgroundPostoperative cognitive decline (PCD) requires microglial activation. Voltage-gated Kv1.3 potassium channels are involved in microglial activation. We determined the role of Kv1.3 in PCD and the efficacy and safety of inhibiting Kv1.3 with phenoxyalkoxypsoralen-1 (PAP-1) in preventing PCD in a mouse model.

methodsAfter institutional approval, we assessed whether Kv1.3-deficient mice (Kv1.3

resultsFreezing behaviour was unaltered in postoperative Kv1.3

conclusionsMicroglial-mediated PCD requires Kv1.3 activity, determined by genetic and pharmacological targeting approaches. Phenoxyalkoxypsoralen-1 blockade of Kv1.3 prevented surgery-induced hippocampal microglial activation and neuroinflammation in mice known to be vulnerable to PCD. Regarding perioperative safety, these beneficial effects of PAP-1 treatment occurred without impacting fracture healing. Kv1.3 blockers, currently undergoing clinical trials for other conditions, may represent an effective and safe intervention to prevent PCD.

Indexed as

AnimalsCognitive DysfunctionDisease Models, AnimalEncephalitisKv1.3 Potassium ChannelMicePostoperative ComplicationsWound HealingKv1.3 Potassium ChannelKv1.3microglial activationneuroinflammationphenoxyalkoxypsoralen-1postoperative cognitive declinepotassium channelwound healing

Identifiers

PMID32624183
PMCPMC7497028
OpenAlexW3040660054

What OpenQuestion holds

Textmetadata
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.