Division of Pulmonary, Allergy, and Critical Care Medicine and.
Division of Pulmonary, Allergy, and Critical Care Medicine and; Department of Medicine, University of Alabama at Birmingham, Birmingham, Alabama.
Am J Med Sci. 2019 May;357(5):384-389. doi: 10.1016/j.amjms.2019.02.008. Epub 2019 Feb 12.
Idiopathic pulmonary fibrosis (IPF) is one of many clinical syndromes that are associated with aging, and is increasing in both incidence and prevalence with the rapid rise in aging populations world-wide. There is accumulating data on how the biology of aging may influence the susceptibility to lung fibrosis in the elderly. In this review, we explore some of the known "hallmarks of aging," including telomere attrition, genomic instability, epigenetic alterations, loss of proteostasis, cellular senescence and mitochondrial dysfunction in the pathobiology of IPF. Additionally, we discuss age-associated alterations in extracellular matrix that may contribute to the development and/or progression of IPF.
特发性肺纤维化（IPF）是与衰老相关的多种临床综合征之一，随着全球人口老龄化的迅速增加，其发病率和患病率都在上升。关于衰老生物学如何影响老年人患肺纤维化的易感性，已有越来越多的数据。在这篇综述中，我们探讨了 IPF 发病机制中一些已知的“衰老标志”，包括端粒磨损、基因组不稳定性、表观遗传改变、蛋白质稳态丧失、细胞衰老和线粒体功能障碍。此外，我们还讨论了与年龄相关的细胞外基质改变，这些改变可能导致 IPF 的发生和/或进展。
