Format

Send to

Choose Destination
Biochim Biophys Acta Mol Cell Res. 2019 Feb 6. pii: S0167-4889(18)30496-8. doi: 10.1016/j.bbamcr.2019.01.013. [Epub ahead of print]

Autophagy in cardiomyopathies.

Author information

1
Institute of Experimental Pharmacology and Toxicology, University Medical Center Hamburg, Hamburg, Germany; German Centre for Cardiovascular Research, Partner Site Hamburg/Kiel/Lübeck, Hamburg, Germany.
2
Division of Molecular Cardiovascular Biology, The Heart Institute, Cincinnati Children's Hospital, Cincinnati, OH, United States of America.
3
Institute of Experimental Pharmacology and Toxicology, University Medical Center Hamburg, Hamburg, Germany; German Centre for Cardiovascular Research, Partner Site Hamburg/Kiel/Lübeck, Hamburg, Germany. Electronic address: l.carrier@uke.de.

Abstract

Autophagy (greek auto: self; phagein: eating) is a highly conserved process within eukaryotes that degrades long-lived proteins and organelles within lysosomes. Its accurate and constant operation in basal conditions ensures cellular homeostasis by degrading damaged cellular components and thereby acting not only as a quality control but as well as an energy supplier. An increasing body of evidence indicates a major role of autophagy in the regulation of cardiac homeostasis and function. In this review, we describe the different forms of mammalian autophagy, their regulations and monitoring with a specific emphasis on the heart. Furthermore, we address the role of autophagy in several forms of cardiomyopathy and the options for therapy.

KEYWORDS:

Autophagosome; Autophagy; Cardiomyopathy; Heart; Lysosome

Supplemental Content

Full text links

Icon for Elsevier Science
Loading ...
Support Center