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First glance at myeloid leukaemia factor 2 in cardiomyocytes

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...

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Main Authors: Voran, Jakob Christoph (Author) , Kilian, Lucia Sophie (Author) , Martini, Simone (Author) , Luzarowski, Marcin (Author) , Noormalal, Marie Isabel (Author) , Müller, Oliver Josef (Author) , Rangrez, Ashraf Yusuf (Author) , Frank, Derk (Author)
Format: Article (Journal)
Language:English
Published: 2026
In: Journal of cardiovascular development and disease
Year: 2026, Volume: 13, Issue: 1, Pages: 1-19
ISSN:2308-3425
DOI:10.3390/jcdd13010019
Online Access:Verlag, kostenfrei, Volltext: https://doi.org/10.3390/jcdd13010019
Verlag, kostenfrei, Volltext: https://www.mdpi.com/2308-3425/13/1/19
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Author Notes:Jakob Christoph Voran, Lucia Sophie Kilian, Simone Martini, Marcin Luzarowski, Marie Isabel Noormalal, Oliver Josef Müller, Ashraf Yusuf Rangrez and Derk Frank
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Summary: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.
Item Description:Veröffentlicht: 30 December 2025
Gesehen am 24.03.2026
Physical Description:Online Resource
ISSN:2308-3425
DOI:10.3390/jcdd13010019

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