Evidence map›Paper›PMID 41590846›Full record

ArticleJournal of cardiovascular development and disease2025

First Glance at Myeloid Leukaemia Factor 2 in Cardiomyocytes.

Jakob Christoph Voran, Lucia Sophie Kilian, Simone Martini, Marcin Luzarowski, Marie Isabel Noormalal, Oliver Josef Müller, Ashraf Yusuf Rangrez, Derk Frank

Abstract read
In one paragraph

Article in Journal of cardiovascular development and disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. Alkylamidobetaines Induced Changes in Multidrug-Resistant, BiofilmingInternational journal of molecular sciences · 2026
    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

8 authors.

Jakob Christoph VoranDepartment of Internal Medicine III, Cardiology and Critical Care, University Hospital Schleswig-Holstein, Campus Kiel, 24105 Kiel, Germany.ORCID 0009-0000-4547-9260
Lucia Sophie KilianDepartment of Internal Medicine III, Cardiology and Critical Care, University Hospital Schleswig-Holstein, Campus Kiel, 24105 Kiel, Germany.
Simone MartiniDepartment of Internal Medicine III, Cardiology and Critical Care, University Hospital Schleswig-Holstein, Campus Kiel, 24105 Kiel, Germany.
Marcin LuzarowskiCore Facility for Mass Spectrometry and Proteomics, Center for Molecular Biology at Heidelberg University (ZMBH), 69120 Heidelberg, Germany.ORCID 0000-0002-2115-0468
Marie Isabel NoormalalDepartment of Internal Medicine III, Cardiology and Critical Care, University Hospital Schleswig-Holstein, Campus Kiel, 24105 Kiel, Germany.
Oliver Josef MüllerGerman Centre for Cardiovascular Research (DZHK), Partner Site Hamburg/Kiel/Lübeck, 24105 Kiel, Germany.ORCID 0000-0001-8223-2638
Ashraf Yusuf RangrezDepartment of Cardiology, Angiology and Pneumology, Universitätsklinikum Heidelberg, Im Neuenheimer Feld 410, 69120 Heidelberg, Germany.ORCID 0000-0003-2630-9754
Derk FrankDepartment of Internal Medicine III, Cardiology and Critical Care, University Hospital Schleswig-Holstein, Campus Kiel, 24105 Kiel, Germany.ORCID 0000-0001-7561-075X

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Understanding the molecular mechanisms that maintain protein homeostasis in cardiomyocytes is fundamental for the development of causal therapies for heart failure. Chaperones, the ubiquitin-proteasome system and autophagy are major regulators of cardiac homeostasis and are crucial for cardiomyocyte function and survival. In this context, myeloid leukaemia factor 2 (MLF2) emerged as a candidate of interest, as we found it overrepresented in protein aggregates in the hearts of mouse models of desmin-related cardiomyopathies (DRM), and it has also been suggested to be associated with dilated cardiomyopathy (DCM). Here, we identified αB-crystallin (CryAB), among other proteins, as a potential interaction partner of MLF2. Functionally, MLF2 was significantly upregulated in mouse models of heart failure and in two in vitro models of cardiomyocyte hypertrophy, and its overexpression resulted in attenuation of pro-hypertrophic gene expression. Taken together, these findings provide initial evidence supporting a role for MLF2 in regulating protein homeostasis and in modulating hypertrophic signalling in cardiomyocytes.

Indexed as

cardiomyocytedesmin-related myopathymyeloid leukaemia factor-2protein aggregates

Identifiers

PMID41590846
PMCPMC12841798

What OpenQuestion holds

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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.