Cantor Jerome
School of Pharmacy and Allied Health Sciences, St. John's University, 8000 Utopia Parkway, Queens, NY 11439, USA.
Life (Basel). 2025 Feb 24;15(3):356. doi: 10.3390/life15030356.
The degradation of elastic fibers is a fundamental characteristic of pulmonary emphysema, resulting in the release of proinflammatory elastin peptides. The findings discussed in this paper support the hypothesis that these peptides act as carriers of disease, interacting with elastin receptor complexes that promote inflammation, elastic fiber damage, and airspace enlargement. Studies from our laboratory show that the breakdown of these fibers is significantly enhanced by intratracheal instillation of elastin peptides in a lipopolysaccharide-induced model of acute lung injury. This result is consistent with a mechanism of elastic fiber injury in which an expanding pool of elastin peptides generates further elastolysis. The accelerating release of the peptides results in a self-perpetuating disease process with the features of an epidemic, where self-replicating agents spread disease. As in the case of an epidemic, elastin peptides resemble disease vectors that transmit alveolar wall injury throughout the lung. This concept may provide a framework for developing novel therapeutic approaches specifically designed to protect elastic fibers from various enzymatic and oxidative insults, thereby slowing the progression of a disease with no robust treatment options.
弹性纤维的降解是肺气肿的一个基本特征，会导致促炎弹性蛋白肽的释放。本文所讨论的研究结果支持这样一种假说，即这些肽作为疾病载体，与促进炎症、弹性纤维损伤和肺泡腔扩大的弹性蛋白受体复合物相互作用。我们实验室的研究表明，在脂多糖诱导的急性肺损伤模型中，气管内注入弹性蛋白肽可显著增强这些纤维的分解。这一结果与弹性纤维损伤机制一致，即不断增加的弹性蛋白肽池会引发进一步的弹性蛋白分解。肽的加速释放导致了一个具有流行病特征的自我延续的疾病过程，其中自我复制因子传播疾病。与流行病的情况一样，弹性蛋白肽类似于在整个肺部传播肺泡壁损伤的疾病载体。这一概念可能为开发新的治疗方法提供一个框架，这些方法专门设计用于保护弹性纤维免受各种酶和氧化损伤，从而减缓这种目前尚无有效治疗方案的疾病的进展。
