Heat shock proteins in pulmonary fibrosis: pawns of cell homeostasis

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.

Automated summary

This review examines the roles of specific heat shock proteins (HSPs), including HSP90, HSP70, and HSP47, in the pathogenesis of idiopathic pulmonary fibrosis (IPF). Understanding the functions of these HSPs in the development of IPF can provide valuable insights for the future treatment and prevention of IPF.