Journal
BIOMOLECULES
Volume 5, Issue 4, Pages 2619-2642Publisher
MDPI
DOI: 10.3390/biom5042619
Keywords
alcohol; mitochondria; mitophagy; autophagy; Parkin; liver injury
Categories
Funding
- NCRR NIH HHS [P20 RR021940, 5P20RR021940] Funding Source: Medline
- NIAAA NIH HHS [R01AA020518, R01 AA020518] Funding Source: Medline
- NIDDK NIH HHS [R01 DK102142] Funding Source: Medline
- NIEHS NIH HHS [T32 ES007079] Funding Source: Medline
- NIGMS NIH HHS [P20 GM103549, P20 GM103418, 8P20 GM103549] Funding Source: Medline
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Alcoholic liver disease (ALD) is a major health problem worldwide, and alcohol is well-known to cause mitochondrial damage, which exacerbates alcohol-induced liver injury and steatosis. No successful treatments are currently available for treating ALD. Therefore, a better understanding of mechanisms involved in regulation of mitochondrial homeostasis in the liver and how these mechanisms may protect against alcohol-induced liver disease is needed for future development of better therapeutic options for ALD. Mitophagy is a key mechanism for maintaining mitochondrial homeostasis by removing damaged mitochondria, and mitophagy protects against alcohol-induced liver injury. Parkin, an E3 ubiquitin ligase, is well-known to induce mitophagy in in vitro models although Parkin-independent mechanisms for mitophagy induction also exist. In this review, we discuss the roles of Parkin and mitophagy in protection against alcohol-induced liver injury and steatosis. We also discuss Parkin-independent mechanisms for mitophagy induction, which have not yet been evaluated in the liver but may also potentially have a protective role against ALD. In addition to mitophagy, mitochondrial spheroid formation may also provide a novel mechanism of protection against ALD, but the role of mitochondrial spheroids in protection against ALD progression needs to be further explored. Targeting removal of damaged mitochondria by mitophagy or inducing formation of mitochondrial spheroids may be promising therapeutic options for treatment of ALD.
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