Highly read on nature.com/nm 8 Aug–4 Sept

Would-be dopers may have a new target: the Rev-erb-α protein. Known to regulate sugar and fat metabolism, the nuclear receptor has now been linked to the production and function of mitochondria — the cell's metabolic powerhouses.

A team led by Bart Staels and Hélène Duez, jointly at the Lille II University of Health and Law and the Pasteur Institute in Lille, France, showed that mouse muscle cells lacking Rev-erb-α contain dysfunctional mitochondria, and that mice lacking the gene encoding it, Nr1d1, could not run as fast as normal mice. The reverse occurred when the protein was overexpressed or when a synthetic agonist was given, suggesting that Rev-erb-α could be targeted by drugs to improve exercise capacity by boosting mitochondrial number and function in muscle cells.

Nature Med. 19, 1039–1046 (2013)