Aging and Susceptibility to Pulmonary Disease

• DOI: 10.1002/cphy.c210026
• Publication Date: 2022-06-29T13:57:21Z
• Authors: Julia Budde; Gwen Skloot
• Keywords: Proteostasis; Immunosenescence; Premature aging; Senescence

The lungs are continually subjected to noxious and inert substances, immunologically active, in a constant state of damage repair. This makes the pulmonary system particularly vulnerable diseases aging. Aging can be understood as random molecular that is unrepaired accumulates over time, resulting cellular defects tissue dysfunction. breakdown mechanisms, including stem cell exhaustion, genomic instability, telomere attrition, epigenetic alteration, loss proteostasis, deregulated nutrient sensing, mitochondrial dysfunction, senescence, altered intercellular communication, changes extracellular matrix thought advance aging process itself. Chronic obstructive disease (COPD), idiopathic fibrosis (IPF), cancers illustrate pathologic these mechanisms beyond normal immune becomes less effective with advancing age. There low-level chronic inflammation termed inflammaging which driven by immunosenescence, innate adaptive systems age lead dysregulation decreased effectiveness system. These processes expected form function respiratory system, most notably lung elasticity, decrease muscle strength, increase ventilation-perfusion mismatching, stiffening vasculature. astute clinician aware findings does not often attribute dyspnea alone. Maintaining low threshold investigate for comorbid understanding how presents differently elderly than younger adults improve clinical outcomes. © 2022 American Physiological Society. Compr Physiol 12:3509-3522, 2022.