Aging is a natural process characterized by progressive functional impairment and reduced capacity to respond appropriately to environmental stimuli and injury. The incidence of two common chronic respiratory diseases (chronic obstructive pulmonary disease (COPD) and idiopathic pulmonary fibrosis (IPF)) increases with advanced age. It is plausible, therefore, that abnormal regulation of the mechanisms of normal aging may contribute to the pathobiology of both COPD and IPF. This review discusses the available evidence supporting a number of aging mechanisms, including oxidative stress, telomere length regulation, cellular and immunosenescense, as well as changes in a number of anti-aging molecules and the extra-cellular matrix are abnormal in COPD and/or IPF. A better understanding of these abnormalities may help the design of novel and better therapeutic interventions for these patients.
|Journal||American Journal of Respiratory and Critical Care Medicine|
|Publication status||Published - 2012|