Getting to the core of fibrosis: targeting redox imbalance in aging

There has been recent progress in the development of anti-fibrotic drugs for the treatment of idiopathic pulmonary fibrosis (IPF) (1,2). Interestingly, the precise mechanisms of action of these drugs are not known (3). Importantly, although both drugs have been shown to slow the progression of disease, neither has been shown to definitively improve quality of life or survival. Clearly, improved therapies for the treatment of IPF and other fibrotic diseases are needed. It has been suggested that core pathways that mediate fibrosis in multiple organ systems may serve as better targets for anti-fibrotic drug development (4). Liepelt and Tacke (5) recently highlight redox imbalance in the context of aging as one of these core pathways.