Deficiency in the zinc transporter ZIP8 impairs epithelia renewal and enhances lung fibrosis.

Content Provider	Europe PMC
Author	Foster, Paul S. Tay, Hock L. Oliver, Brian G.
Copyright Year	2022
Abstract	Although aging and lung injury are linked to the development of idiopathic pulmonary fibrosis (IPF), the underlying pathognomonic processes predisposing to fibrotic lesions remain largely unknown. A deficiency in the ability of type 2 alveolar epithelial cell (AEC2) progenitors to regenerate and repair the epithelia has been proposed as a critical factor. In this issue of the JCI, Liang et al. identify a deficiency in the zinc transporter SLC39A8 (ZIP8) in AEC2s and in the subsequent activation of the sirtuin SIRT1 that predisposes to decreased AEC2 renewal capacity and enhanced lung fibrosis in both IPF and aging lungs. Interestingly, the authors demonstrate the efficacy of modulating dietary zinc levels, suggesting the need for clinical trials to evaluate the therapeutic potential of dietary supplementation and the development of pharmacological modulation of the Zn/ZIP8/SIRT1 axis for treatment.
ISSN	00219738
Journal	The Journal of Clinical Investigation
Volume Number	132
PubMed Central reference number	PMC9151685
Issue Number	11
PubMed reference number	35642632
e-ISSN	15588238
DOI	10.1172/JCI160595
Language	English
Publisher	American Society for Clinical Investigation
Publisher Date	2022-06-01
Access Restriction	Open
Rights License	This work is licensed under the Creative Commons Attribution 4.0 International License. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/. © 2022 Foster et al.
Content Type	Text
Resource Type	Article
Subject	Medicine