Dept of Respiratory Medicine, Hospital del Mar - IMIM, DCEXS, Universitat Pompeu Fabra, CIBERES, ISCIII, Barcelona Respiratory Network, Barcelona, Spain
Dept of Respiratory Medicine, Hospital del Mar - IMIM, DCEXS, Universitat Pompeu Fabra, CIBERES, ISCIII, Barcelona Respiratory Network, Barcelona, Spain.
Eur Respir Rev. 2020 Sep 17;29(157). doi: 10.1183/16000617.0087-2020. Print 2020 Sep 30.
Ageing is a progressive condition that usually leads to the loss of physiological properties. This process is also present in respiratory muscles, which are affected by both senescent changes occurring in the whole organism and those that are more specific for muscles. The mechanisms of the latter changes include oxidative stress, decrease in neurotrophic factors and DNA abnormalities. Ageing normally coexists with comorbidities, including respiratory diseases, which further deteriorate the structure and function of respiratory muscles. In this context, changes intrinsic to ageing become enhanced by more specific factors such as the impairment in lung mechanics and gas exchange, exacerbations and hypoxia. Hypoxia in particular has a direct effect on muscles, mainly through the expression of inducible factors (hypoxic-inducible factor), and can result in oxidative stress and changes in DNA, decrease in mitochondrial biogenesis and defects in the tissue repair mechanisms. Intense exercise can also cause damage in respiratory muscles of elderly respiratory patients, but this can be followed by tissue repair and remodelling. However, ageing interferes with muscle repair by tampering with the function of satellite cells, mainly due to oxidative stress, DNA damage and epigenetic mechanisms. In addition to the normal process of ageing, stress-induced premature senescence can also occur, involving changes in the expression of multiple genes but without modifications in telomere length.
衰老是一种渐进的状态，通常会导致生理特性的丧失。这个过程也存在于呼吸肌中，它受到全身衰老变化和更特定于肌肉的变化的影响。后者变化的机制包括氧化应激、神经营养因子减少和 DNA 异常。衰老是常伴有合并症的，包括呼吸系统疾病，这会进一步恶化呼吸肌的结构和功能。在这种情况下，与衰老相关的变化会因更特定的因素而加剧，如肺力学和气体交换的损害、恶化和缺氧。特别是缺氧对肌肉有直接影响，主要通过诱导因子（缺氧诱导因子）的表达，并且会导致氧化应激和 DNA 变化、线粒体生物发生减少以及组织修复机制缺陷。剧烈运动也会导致老年呼吸系统疾病患者的呼吸肌损伤，但随后会发生组织修复和重塑。然而，衰老会通过干扰卫星细胞的功能来干扰肌肉修复，主要是由于氧化应激、DNA 损伤和表观遗传机制。除了正常的衰老过程外，还可能发生应激诱导的过早衰老，涉及多个基因表达的变化，但端粒长度没有改变。
