We are working to understand human metabolism and what happens when this biological system breaks down. The problem is more important than ever, given the increasing burden that diabetes and other metabolic dysfunctions have on human health and society.

Cracking the case of mitochondrial repair and replacement in metabolic stress

Professor Reuben Shaw has spent nearly two decades piecing together how the cell responds to metabolic stress, which occurs when cellular energy levels dip. Whether energy levels fall because the cell’s powerhouses (mitochondria) are failing or due to a lack of necessary energy-making supplies, the response is the same: get rid of the damaged mitochondria and create new ones. Now, Shaw, first author Nazma Malik, and colleagues crack the case on this process of removal and replacement, finding that a protein called FNIP1 is the critical link between a cell sensing low energy levels and eliminating and replacing damaged mitochondria. The finding has implications for better understanding healthy aging, cancer, neurodegenerative diseases, and more.

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