Evidence map›Paper›PMID 33533257›Full record

ArticleJournal of the American Heart Association2021

MK2-Deficient Mice Are Bradycardic and Display Delayed Hypertrophic Remodeling in Response to a Chronic Increase in Afterload.

Matthieu Ruiz, Maya Khairallah, Dharmendra Dingar, George Vaniotis, Ramzi J Khairallah, Benjamin Lauzier, Simon Thibault, Joëlle Trépanier, Yanfen Shi, Annie Douillette and 12 more

Open access · goldAbstract read
In one paragraph

Article in Journal of the American Heart Association, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.6field-weighted citation impact, top 34% 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

6 citing papers in PubMed, 11 citations in OpenAlex.

  1. Article
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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

22 authors at 5 institutions in 5 countries.

Matthieu RuizDepartment of Medicine Université de Montréal Québec Canada.
Maya KhairallahDepartment of Biochemistry and Molecular Medicine Université de Montréal Québec Canada.
Dharmendra DingarDepartment of Biochemistry and Molecular Medicine Université de Montréal Québec Canada.
George VaniotisDepartment of Biochemistry and Molecular Medicine Université de Montréal Québec Canada.
Ramzi J KhairallahUniversity of Maryland Baltimore MD.
Benjamin LauzierL'Institut du Thorax INSERMCNRSUniversité de Nantes France.
Simon ThibaultFaculté de Pharmacie Université de Montréal Québec Canada.
Joëlle TrépanierDepartment of Biochemistry and Molecular Medicine Université de Montréal Québec Canada.
Yanfen ShiMontreal Heart Institute Montréal Québec Canada.
Annie DouilletteMontreal Heart Institute Montréal Québec Canada.
Bahira HusseinMontreal Heart Institute Montréal Québec Canada.
Sherin Ali NawaitoDepartment of Pharmacology and Physiology Université de Montréal Québec Canada.
Pramod SahadevanDepartment of Biochemistry and Molecular Medicine Université de Montréal Québec Canada.
Albert NguyenDepartment of Pharmacology and Physiology Université de Montréal Québec Canada.
Fatiha SahmiMontreal Heart Institute Montréal Québec Canada.
Marc-Antoine GillisMontreal Heart Institute Montréal Québec Canada.
Martin G SiroisDepartment of Pharmacology and Physiology Université de Montréal Québec Canada.
Matthias GaestelInstitute of Cell BiochemistryHannover Medical School Hannover Germany.
William C StanleyUniversity of Maryland Baltimore MD.
Céline FisetFaculté de Pharmacie Université de Montréal Québec Canada.
Jean-Claude TardifDepartment of Medicine Université de Montréal Québec Canada.
Bruce G AllenDepartment of Medicine Université de Montréal Québec Canada.
Montreal Heart Institute · CAUniversity of Maryland, Baltimore · USCentre National de la Recherche Scientifique · FRMedizinische Hochschule Hannover · DESuez Canal University · EG

Funding

CIHR MOP‐77791
6 · The paper itself

Abstract

Background Mitogen-activated protein kinase-activated protein kinase-2 (MK2) is a protein serine/threonine kinase activated by p38α/β. Herein, we examine the cardiac phenotype of pan MK2-null (MK2

Indexed as

Ventricular RemodelingAnimalsBlood PressureBradycardiaCardiomyopathy, HypertrophicHeart RateIntracellular Signaling Peptides and ProteinsMaleMAP-Kinase-Activated Kinase 2MiceMice, Inbred C57BLMice, TransgenicMitochondria, HeartProtein Serine-Threonine KinasesVentricular Function, LeftIntracellular Signaling Peptides and ProteinsMAP-Kinase-Activated Kinase 2Protein Serine-Threonine Kinasesbradycardiacardiac remodelingmitochondrial permeability transition poreMK2p38 MAPK

Identifiers

PMID33533257
PMCPMC7955338
OpenAlexW3127001377

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.