This is an addendum to a recent report which demonstrates for the first time that autophagic flux is increased in the heart of a well-established mouse model of cardiac proteinopathy and p62 is transcriptionally upregulated in cardiomyocytes and hearts overexpressing human cardiomyopathy-linked misfolded proteins. The p62 plays a critical and protective role in aggresome formation and autophagic activation in cardiomyocytes overexpressing misfolded proteins.
- Desmin-related cardiomyopathy
- Protein aggregation
ASJC Scopus subject areas
- Molecular Biology
- Cell Biology