Fibroblasts and their responses to chronic injury in pulmonary fibrosis

B Wu; L Tang; M Kapoor

doi:10.1016/j.semarthrit.2020.12.003

Fibroblasts and their responses to chronic injury in pulmonary fibrosis

Semin Arthritis Rheum. 2021 Feb;51(1):310-317. doi: 10.1016/j.semarthrit.2020.12.003. Epub 2020 Dec 10.

Authors

B Wu¹, L Tang¹, M Kapoor²

Affiliations

¹ Schroeder Arthritis Institute, University Health Network, Toronto, Ontario, Canada; Krembil Research Institute, University Health Network, Toronto, Ontario, Canada; Departments of Surgery and of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, Ontario, Canada.
² Schroeder Arthritis Institute, University Health Network, Toronto, Ontario, Canada; Krembil Research Institute, University Health Network, Toronto, Ontario, Canada; Departments of Surgery and of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, Ontario, Canada. Electronic address: mkapoor@uhnresearch.ca.

PMID: 33440304
DOI: 10.1016/j.semarthrit.2020.12.003

Abstract

The field of pulmonary fibrosis is rapidly expanding as new insights highlight novel mechanisms that influence fibroblast biology and likely promote aberrant and chronic activation of the tissue repair response. Current paradigms suggest repeated epithelial microinjury as a driver for pathology; however, the rapid expansion of pulmonary fibrosis research calls for an overview on how fibroblasts respond to both neighbouring cells and the injury microenvironment. This review seeks to highlight recent discoveries and identify areas that require further research regarding fibroblasts, and their role in pulmonary fibrosis.

Keywords: Autophagy; Cell-cell interaction; Fibroblast; Fibroblast senescence; Oxidative stress; Pulmonary fibrosis.

Publication types

Research Support, Non-U.S. Gov't
Review

MeSH terms

Cellular Senescence
Fibroblasts
Humans
Idiopathic Pulmonary Fibrosis*

Grants and funding

434790/CIHR/Canada