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HOPE for FATIGUE

New Findings Reveal Mitochondria May Instigate Lupus-like Inflammation

Targeting mitochondria metabolism may hold hope for new Lupus treatments. According to researchers at University of Washington who have discovered that the inflammation characteristic of lupus could be brought on by the release of mitochondrial byproducts (reactive oxygen species-ROS) that are released into web-like traps created by white blood cells (neutrophils) whose job is to capture bacteria and pathogens in the blood.

While these traps known as NETs (neutrophil extracellular traps), can be life saving in capturing pathogens, excessive NET formation can be damaging to tissue and cause cells to die in a process called NETosis. Previous studies have shown that NETs contribute to lupus pathology, and drugs that inhibit NET formation improve lupus symptoms in mouse models of the disease.

Authors of a recent study entitled, "Neutrophil extracellular traps enriched in oxidized mitochondria DNA are interferogenic and contribute to lupus-llike disease," stress that ongoing study of mitochondrial ROS in NET formation and autoimmunity offers new hope for treatments of autoimmune diseases like lupus.

Publication

Lood, C., Blanco, L. P., Purmalek, M. M., Carmona-Rivera, C., De Ravin, S. S., Smith, C. K., ... & Kaplan, M. J. (2016). Neutrophil extracellular traps enriched in oxidized mitochondrial DNA are interferogenic and contribute to lupus-like disease. Nature medicine.

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