You are currently viewing the editor's summary.
View Full TextLog in to view the full text
AAAS login provides access to Science for AAAS members, and access to other journals in the Science family to users who have purchased individual subscriptions.
Register for free to read this article
As a service to the community, this article is available for free. Existing users log in.
More options
Download and print this article for your personal scholarly, research, and educational use.
Buy a single issue of Science for just $15 USD.
Two-Face Chitinase
Idiopathic pulmonary fibrosis is a devastating—currently incurable—disease where scars develop deep in the lung, making it hard to breathe. Now, Zhou et al. report a breath of fresh air for IPF. They found that the protein chitinase 3–like 1 (CHI3L1) is elevated in IPF patients, and that high levels of CHI3L1 are associated with disease progression. However, things were not as simple as they seemed. CHI3L1 actually played a protective, anti-apoptotic role against lung injury, but contributed to fibrosis during the repair phase, in part through inducing myofibroblast transformation. This insight into the two sides of CHI3L1 provides mechanistic understanding of the pathogenesis of IPF, which is necessary to the development of successful therapeutics.
- Copyright © 2014, American Association for the Advancement of Science
