New Study Illuminates Mechanism for Elimination of Damaged Mitochondria

Researchers at the University of Texas (UT) Southwestern Medical Center have illuminated the mechanism cells use to find and destroy damaged mitochondria that, when damaged, may lead to genetic problems, cancer, neurodegenerative diseases, inflammatory disease, and aging. Understanding how this process works could potentially lead to new treatments to prevent certain illnesses and even some aspects of aging, said Dr. Beth Levine, Director of the Center for Autophagy Research at UT Southwestern and senior author of the study, which was published online on December 22, 2016 in Cell. The Center for Autophagy Research – the only one of its kind in the nation – investigates the process called autophagy in which cells rid themselves of damaged or unnecessary components. Mitochondria are commonly called the “powerhouses of the cell” because they work like tiny factories inside cells to convert compounds such as sugars into energy that a cell can use. But mitochondria also have a dark side: Because of their high-energy function, when they are damaged, they release toxic chemicals called reactive oxygen species into the rest of the cell, said Dr. Yongjie Wei, Assistant Professor of Internal Medicine at UT Southwestern and lead co-first author of the study. “The removal of damaged mitochondria by autophagy (a process called mitophagy) is important for cellular health,” said Dr. Levine, also Professor of Internal Medicine and Microbiology and a Howard Hughes Medical Institute (HHMI) Investigator. Researchers have, to date, focused on protein “tags” found on the outer membranes of mitochondria – especially the protein Parkin that attaches these tags – to explain how the cell’s degradative organelles, called autophagosomes, target sick mitochondria, explained Dr. Levine, who holds the Charles Cameron Sprague Distinguished Chair in Biomedical Science.
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