Evidence map›Paper›PMID 28481959›Full record

ArticlePloS one2017

TRPV2 knockout mice demonstrate an improved cardiac performance following myocardial infarction due to attenuated activity of peri-infarct macrophages.

Michal Entin-Meer, Lena Cohen, Einat Hertzberg-Bigelman, Ran Levy, Jeremy Ben-Shoshan, Gad Keren

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.6field-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

25 citing papers in PubMed, 49 citations in OpenAlex.

  1. Trial
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  8. Article
  9. Macrophages in myocardial infarction.American journal of physiology. Cell physiology · 2022
    Review
  10. Article
  11. Review
  12. Review
  13. Review
  14. Review
  15. Flotillin-1 Interacts With and Sustains the Surface Levels of TRPV2 Channel.Frontiers in cell and developmental biology · 2021
    Article
  16. TRPV2 channel as a possible drug target for the treatment of heart failure.Laboratory investigation; a journal of technical methods and pathology · 2020
    Review
  17. Article
  18. Targeting CaFrontiers in physiology · 2020
    Review
  19. Article
  20. Oxidation of methionine residues activates the high-threshold heat-sensitive ion channel TRPV2.Proceedings of the National Academy of Sciences of the United States of America · 2019
    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

6 authors at 2 institutions in 1 country.

Michal Entin-MeerThe Laboratory of Cardiovascular Research, Department of Cardiology, Tel-Aviv Sourasky Medical Center, Tel-Aviv, Israel.ORCID http://orcid.org/0000-0001-9909-5502
Lena CohenThe Laboratory of Cardiovascular Research, Department of Cardiology, Tel-Aviv Sourasky Medical Center, Tel-Aviv, Israel.
Einat Hertzberg-BigelmanThe Laboratory of Cardiovascular Research, Department of Cardiology, Tel-Aviv Sourasky Medical Center, Tel-Aviv, Israel.
Ran LevyThe Laboratory of Cardiovascular Research, Department of Cardiology, Tel-Aviv Sourasky Medical Center, Tel-Aviv, Israel.
Jeremy Ben-ShoshanThe Laboratory of Cardiovascular Research, Department of Cardiology, Tel-Aviv Sourasky Medical Center, Tel-Aviv, Israel.
Gad KerenThe Laboratory of Cardiovascular Research, Department of Cardiology, Tel-Aviv Sourasky Medical Center, Tel-Aviv, Israel.
Tel Aviv University · ILTel Aviv Sourasky Medical Center · IL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundWe have recently shown that the expression of the transient receptor potential vanilloid 2 channel, TRPV2, is upregulated in the peri-infarct zone 3-5 days following an acute myocardial infarction (AMI). Further analysis has demonstrated that invading monocytes maturing to macrophages merely harbor the documented elevated expression of this channel. PURPOSE: Assess cardiac function in TRPV2-KO mice compared to TRPV2-WT following AMI and analyze the potential involvement of TRPV2-expressing macrophages in the recovery process.

methodsTRPV2-KO or WT mice were induced with AMI by ligation of the left anterior descending artery (LAD). In another set of experiments, TRPV2-KO mice induced with AMI, were intravenously (IV) injected with WT or TRPV2-KO peritoneal macrophages in order to directly assess the potential contribution of TRPV2-expressing macrophages to cardiac healing. Cardiac parameters were obtained by echocardiography 1 day and 30 days post infarction. The relative changes in the ejection fraction (EF) and additional cardiac parameters between baseline (day 1) and day 30 were calculated and statistical significance was determined (SPSS).

resultsThe in vivo study showed that while EF was significantly decreased in the WT animals between baseline and day 30, EF was only slightly and insignificantly reduced in the KO animals. Likewise LVESD and LVESA were significantly modified exclusively in the WT animals. Moreover, intravenous administration of peritoneal WT macrophages, but not KO macrophages, significantly reduced survival of post-MI TRPV2-KO mice.

conclusionThe data suggest that knockout of the TRPV2 channel may attenuate macrophage-dependent pro-inflammatory processes and result in better cardiac recovery. TRPV2 may thus represent a novel therapeutic target for treatment of patients undergoing an acute MI.

Indexed as

AnimalsCalcium ChannelsMacrophages, PeritonealMiceMice, KnockoutMyocardial InfarctionTRPV Cation ChannelsCalcium ChannelsTrpv2 protein, mouseTRPV Cation Channels

Identifiers

PMID28481959
PMCPMC5421795
OpenAlexW2612900737

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Registered trials

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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.