Chronic lung diseases are diseases of the elderly and mechanisms that link aging with the pathogenesis of lung disease have recently been discovered. In particular, over the last decade, accumulating evidence has suggested a causative link between mitochondrial dysfunction and major phenotypes associated with aging, such as inflammation, tissue remodeling, and aberrant wound repair. Thus mitochondrial dysfunction has become a focus for our understanding of lung aging and disease mechanisms and the potential of reprogramming mitochondria function for the development of new therapies is emerging. This integrated symposium highlights emerging understanding of the breadth and integrated pathobiological responses of mitochondria during aging and disease, how these may contribute to lung tissue destruction, and potential for this knowledge to inform development of mitochondria-reprogramming therapies.