Division of Pulmonary, Allergy and Critical Care, Department of Medicine, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania.
Am J Physiol Cell Physiol. 2022 Jun 1;322(6):C1105-C1109. doi: 10.1152/ajpcell.00073.2022. Epub 2022 May 4.
Idiopathic pulmonary fibrosis (IPF) is a fatal disease that primarily affects the elderly. Up to date, the specific pathogenesis of IPF remains unknown. However, it is theorized to be caused by chronic repetitive injuries to the alveolar epithelium, eventually exhausting the stem cell capacity and activating pathological pathways. Heat shock proteins (HSPs), a category of stress response proteins, are also suggested to contribute to IPF pathogenesis. Furthermore, HSPs are key components in the regulation of cell homeostasis and act as chaperones for a multitude of new proteins. This review thoroughly evaluates the roles that specific HSPs, HSP90, HSP70, and HSP47, have in the fibrotic process. A close look into the roles of these HSPs in IPF pathogenesis will give valuable insight into the future of IPF treatment and prevention.
特发性肺纤维化（IPF）是一种主要影响老年人的致命疾病。迄今为止，IPF 的具体发病机制尚不清楚。然而，据推测是由肺泡上皮的慢性反复损伤引起的，最终耗尽干细胞能力并激活病理途径。热休克蛋白（HSPs）是应激反应蛋白的一类，也被认为与 IPF 的发病机制有关。此外，HSPs 是细胞内稳态调节的关键组成部分，并且作为多种新蛋白质的伴侣。本综述全面评估了特定 HSPs（HSP90、HSP70 和 HSP47）在纤维化过程中的作用。深入研究这些 HSPs 在 IPF 发病机制中的作用，将为 IPF 的治疗和预防提供有价值的见解。
