Copertina

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...

Descrizione completa

Salvato in:
Dettagli Bibliografici
Autori principali: Voran, Jakob Christoph (Autore) , Kilian, Lucia Sophie (Autore) , Martini, Simone (Autore) , Luzarowski, Marcin (Autore) , Noormalal, Marie Isabel (Autore) , Müller, Oliver Josef (Autore) , Rangrez, Ashraf Yusuf (Autore) , Frank, Derk (Autore)
Natura: Article (Journal)
Lingua:inglese
Pubblicazione: 2026
In: Journal of cardiovascular development and disease
Year: 2026, Volume: 13, Fascicolo: 1, Pages: 1-19
ISSN:2308-3425
DOI:10.3390/jcdd13010019
Accesso online:Verlag, kostenfrei, Volltext: https://doi.org/10.3390/jcdd13010019
Verlag, kostenfrei, Volltext: https://www.mdpi.com/2308-3425/13/1/19
Testo
Note sull'autore:Jakob Christoph Voran, Lucia Sophie Kilian, Simone Martini, Marcin Luzarowski, Marie Isabel Noormalal, Oliver Josef Müller, Ashraf Yusuf Rangrez and Derk Frank
Descrizione
Riassunto: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.
Descrizione del documento:Veröffentlicht: 30 December 2025
Gesehen am 24.03.2026
Descrizione fisica:Online Resource
ISSN:2308-3425
DOI:10.3390/jcdd13010019

Documenti analoghi