Press Release


Can aspartate treatment revert defective protein turnover?

Scientists of ILBD/CPC uncover unexpected consequences of defective mitochondrial metabolism

A fundamental novel cell biological mechanism was discovered in the group of Prof. Dr. Silke Meiners, Institute of Lung Biology and Disease (ILBD)/Comprehensive Pneumology Center (CPC). The group uncovered how mitochondrial metabolism adaptively adjusts protein turnover in the cell. Specifically, they showed that the metabolic reprogramming of the mitochondria results in the  deficiency of a single amino acid, i.e. aspartate, which reduces both, protein synthesis and protein degradation in the cell. Supplementation of aspartate restores protein synthesis and also activates the assembly of the main protein degrading machinery of the cell, the proteasome. The study thus uncovers unexpected consequences of defective mitochondrial metabolism in aging and disease for the overall protein turnover in the cell. As aspartate treatment can revert defective protein turnover, these results have therapeutic implications.

Silke Meiners: “We assume that this finding is relevant for all chronic diseases, in which mitochondrial function is restricted. These include diseases with genetic mutations of mitochondrial genes but also metabolic diseases involving mitochondrial dysfunction such as cancer, diabetes and chronic lung diseases as well as aging. Our lab is currently investigating how the metabolic regulation of protein turnover contributes to idiopathic pulmonary fibrosis."

Link to the publication