Mitochondria in Liver Pathobiology

Dear Colleagues,

As the second-largest organ of the body after the skin, the liver has many important metabolic functions. Consequently, many pathological events can occur in this organ. Frequently, mitochondria play a key pathogenic role in liver disease. As a major site of reactive oxygen species (ROS) production, mitochondria are implicated in the pathogenesis of alcoholic and nonalcoholic liver disease, as actively investigated by several research groups.

Mitochondrial autophagy, or mitophagy, is the process of autophagic sequestration and lysosomal degradation of mitochondria that occurs in response to nutrient deprivation, mitochondrial damage, and cellular remodeling. Timely and well-orchestrated removal of damaged mitochondria by mitophagy is crucial for cellular homeostasis and function. Inadequate or disordered mitophagy promotes oxidative stress, cell injury, and the pathogenesis of many diseases, including those that occur in the liver. By contrast, overactive mitophagy can produce mitochondrial depletion and bioenergetic deficits.

Mitochondria are also the site of biosynthesis of heme and Fe–S clusters. Substantial evidence also implicates mitochondrial iron as an important contributor to liver pathology, including acetaminophen hepatotoxicity, ischemia-reperfusion, oxidative stress, and iron overload in hemochromatosis. Toxicity from redox-active iron can occur by the Fenton reaction producing hydroxy radical, a highly toxic ROS. Given the central role of mitochondria in ROS generation, mitochondrial iron must be tightly regulated to provide a sufficient supply of iron for processes for which iron is a co-factor but at the same time prevent the formation of toxic ROS.

These are just a few examples of how mitochondria can play a key role in the pathobiology of the liver.

We encourage all research groups working in the areas related to mitochondria and liver pathobiology to make contributions to this Special Issue.

Dr. Anna-Liisa Nieminen
Prof. John Lemasters
Guest Editors

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• alcohol
• cell death
• liver
• iron
• mitochondria
• mitophagy
• NAFLD/NASH
• oxidative stress