Journal
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE
Volume 1865, Issue 4, Pages 797-809Publisher
ELSEVIER
DOI: 10.1016/j.bbadis.2018.09.034
Keywords
Autophagy; Mitophagy; PINK1; PARKIN; BNIP3; NIX; RAB5
Funding
- NTH [NTH R21AG052280, R01HL132300, R01HL138560, P01HL085577]
- NIH F31 Predoctoral Fellowship [5F31HL136228]
- AHA Established Investigator Award
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The heart is composed of cardiomyocytes that require large amounts of energy to sustain contraction. Mitochondria are distinctive organelles of bacterial origin that generate most of the energy for the heart via oxidative phosphorylation. To ensure a healthy population of mitochondria that efficiently produce ATP, myocytes quickly eliminate any unhealthy or unwanted mitochondria via a process known as mitochondrial autophagy, or mitophagy. It is especially important to selectively remove damaged or aged mitochondria since they can become excessive producers of reactive oxygen species and release pro-death proteins. Because this is such a crucial cellular process, cells have several mechanisms in place to deal with potentially harmful mitochondria. Here, we review the various pathways identified to date and how they are regulated. We also discuss the importance of these canonical and non-canonical pathways in the heart and their link to cardiovascular health, disease and aging.
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