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Modulating Copper Reactivity: A New Approach to Reprogram Mitochondrial Retrograde Signaling
Emmanouil Zacharioudakis1,2,3,4,5
1Department of Biochemistry, Albert Einstein College of Medicine, Bronx, New York 10461, United States of America.
Abstract:
The crosstalk between mitochondria and the nucleus regulates cell plasticity and innate immune response. A new study shows that copper(II) accumulates in mitochondria of activated macrophages in response to pathogen infection and induces metabolic and epigenetic reprogramming that promotes inflammation. Pharmacologic targeting of mitochondrial copper(II) uncovers a new therapeutic strategy to combat aberrant inflammation and regulate cell plasticity.
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