MLF2 was significantly upregulated in mouse models of heart failure, where its overexpression attenuated pro-hypertrophic gene expression.
MLF2 interacts with αB-crystallin and its overexpression attenuates pro-hypertrophic gene expression, suggesting a role in regulating protein homeostasis and modulating hypertrophic signaling in cardiomyocytes.
Absolute Event Rate: 0% vs 0%
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.
Voran et al. (Tue,) reported a other. MLF2 was significantly upregulated in mouse models of heart failure, where its overexpression attenuated pro-hypertrophic gene expression.
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