Evidence map›Paper›PMID 38516190›Full record

ArticleFrontiers in molecular biosciences2024

Genetic ablation of Lmp2 increases the susceptibility for impaired cardiac function.

Felix A Trogisch, Franziska Koser, Synje Michel, David A Liem, Bogdan I Florea, Markus Hecker, Oliver Drews

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Frontiers in molecular biosciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact, top 96% 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

0 citing papers in PubMed, 0 citations in OpenAlex.

No citing paper in PubMed yet.

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

7 authors at 5 institutions in 4 countries.

Felix A TrogischEuropean Center for Angioscience, Department of Cardiovascular Physiology, Mannheim Medical Faculty, Heidelberg University, Mannheim, Germany.
Franziska KoserDepartment of Cardiovascular Physiology, Institute of Physiology and Pathophysiology, Heidelberg University, Heidelberg, Germany.
Synje MichelDepartment of Cardiovascular Physiology, Institute of Physiology and Pathophysiology, Heidelberg University, Heidelberg, Germany.
David A LiemDepartments of Physiology and Medicine/Cardiology, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA, United States.
Bogdan I FloreaLeiden Institute of Chemistry, Leiden University, Leiden, Netherlands.
Markus HeckerDepartment of Cardiovascular Physiology, Institute of Physiology and Pathophysiology, Heidelberg University, Heidelberg, Germany.
Oliver DrewsDepartment of Cardiovascular Physiology, Institute of Physiology and Pathophysiology, Heidelberg University, Heidelberg, Germany.
Heidelberg University · DEJohannes Kepler University of Linz · ATLeiden University · NLUniversity Hospital Heidelberg · DEUniversity of California, Los Angeles · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Proteasome degradation is an integral part of cellular growth and function. Proteasomal intervention may mitigate adverse myocardial remodeling, but is associated with the onset of heart failure. Previously, we have demonstrated that increasing abundance of cardiac Lmp2 and its incorporation into proteasome complexes is an endogenous mechanism for proteasome regulation during hypertrophic remodeling of the heart induced by chronic

Indexed as

adverse cardiac effectscardiac remodelingheart failureproteasome interventionproteostasisubiquitin-proteasome system

Identifiers

PMID38516190
PMCPMC10955435
OpenAlexW4392558258

What OpenQuestion holds

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LicenceCC BY
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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.