Evidence map›Paper›PMID 31511966›Full record

ArticlePflugers Archiv : European journal of physiology2019

TREK-1 protects the heart against ischemia-reperfusion-induced injury and from adverse remodeling after myocardial infarction.

Samuel Kamatham, Christopher M Waters, Andreas Schwingshackl, Salvatore Mancarella

Open access · greenAbstract read
In one paragraph

Article in Pflugers Archiv : European journal of physiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.3field-weighted citation impact, top 18% 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

17 citing papers in PubMed, 19 citations in OpenAlex.

  1. Review
  2. Article
  3. KPharmaceuticals (Basel, Switzerland) · 2026
    Review
  4. The two-pore KAmerican journal of physiology. Heart and circulatory physiology · 2025
    Article
  5. Article
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  9. Cardiomyocyte-Specific Wt1 Is Involved in Cardiac Metabolism and Response to Damage.Journal of cardiovascular development and disease · 2023
    Article
  10. Review
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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

4 authors at 3 institutions in 1 country.

Samuel KamathamDepartment of Physiology, University of Tennessee Health Sciences Center, 71 S. Manassas Street, Memphis, TN, 38163, USA.
Christopher M WatersDepartment of Physiology, Saha Cardiovascular Research Center, University of Kentucky, Lexington, KY, USA.
Andreas SchwingshacklDepartment of Pediatrics, University of California Los Angeles, Los Angeles, CA, USA.
Salvatore MancarellaDepartment of Physiology, University of Tennessee Health Sciences Center, 71 S. Manassas Street, Memphis, TN, 38163, USA. smancare@uthsc.edu.ORCID 0000-0001-9049-4697
University of Tennessee Health Science Center · USUniversity of California, Los Angeles · USUniversity of Kentucky · US

Funding

ASK1 and Ventilator-Induced Lung InjuryR01HL131526 · NHLBI · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI WATERS, CHRISTOPHER M · 2017 to 2020
$1.7M
CXCR4 signaling in lung epithelial repairR01HL123540 · NHLBI · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI WATERS, CHRISTOPHER M · 2014 to 2017
$1.5M
STIM-Dependent Signaling in Cardiac PathophysiologyR00HL114869 · NHLBI · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI MANCARELLA, SALVATORE · 2016 to 2018
$738k
STIM-Dependent Signaling in Cardiac PathophysiologyK99HL114869 · NHLBI · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI MANCARELLA, SALVATORE · 2013 to 2014
$208k
NHLBI NIH HHS HL114869NHLBI NIH HHS K99 HL114869NHLBI NIH HHS R00 HL114869NHLBI NIH HHS R01 HL123540NHLBI NIH HHS R01 HL131526
6 · The paper itself

Abstract

The TWIK-related K+ channel (TREK-1) is a two-pore-domain potassium channel that produces background leaky potassium currents. TREK-1 has a protective role against ischemia-induced neuronal damage. TREK-1 is also expressed in the heart, but its role in myocardial ischemia-reperfusion (IR)-induced injury has not been examined. In the current study, we used a TREK-1 knockout (KO) mouse model to show that TREK-1 has a critical role in the cardiac I/R-induced injury and during remodeling after myocardial infarction (MI). At baseline, TREK-1 KO mice had similar blood pressure and heart rate as the wild-type (WT) mice. However, the lack of TREK-1 was associated with increased susceptibility to ischemic injury and compromised functional recovery following ex vivo I/R-induced injury. TREK-1 deficiency increased infarct size following permanent coronary artery ligation, resulting in greater systolic dysfunction than the WT counterpart. Electrocardiographic (ECG) analysis revealed QT interval prolongation in TREK-1 KO mice, but normal heart rate (HR). Acutely isolated TREK-1 KO cardiomyocytes exhibited prolonged Ca

Indexed as

Action PotentialsAnimalsBlood PressureCalcium SignalingCells, CulturedHeart RateMaleMiceMice, Inbred C57BLMyocardial Reperfusion InjuryMyocytes, CardiacPotassium Channels, Tandem Pore Domainpotassium channel protein TREK-1Potassium Channels, Tandem Pore DomainIschemia-reperfusionMiceMyocardial infarctionPotassium channelTelemetryTREK-1

Identifiers

PMID31511966
PMCPMC8996126
OpenAlexW2972579595

What OpenQuestion holds

Textmetadata
LicenceTDM
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.