Idiopathic pulmonary fibrosis (IPF) is a disease of aging, with progressive lung scarring, and no known cure [1-3]. While the diagnostic criteria for IPF have evolved [3], the mechanisms underlying the aging predilection to IPF are still unclear. Aging is strongly associated with altered mitochondrial bioenergetic functions [4]. IPF lungs are known to have increased cellular senescence associated with metabolic perturbations and altered bioenergetics due to mitochondrial dysfunction [5, 6], which are associated with reduced ATP levels due to imbalance between glycolysis and mitochondrial respiration [6-8]. The causal relationships are unknown.

Here [9], Sui and Boatz et al. report on new insights into a piece of the puzzle, namely epithelial cell senescence in IPF, by exploring the role of the adenine nucleotide translocase-1 (ANT1). Present in abundance in health in the inner mitochondrial membrane, ANTs (4 currently known isoforms, ANT1-4), as their name suggests, exchange ADP/ATP across the inner mitochondrial membrane. It follows that alterations in the function of these proteins could have profound effects on cellular bioenergetics and phenotypes. Indeed, as early as 1997, ANT deficiency was noted to result in mitochondrial myopathy and heart failure [10]. Since then, ANTs have been implicated in diabetes mellitus, Alzheimer’s disease, Parkinson’s disease and other degenerative disorders [11].