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

Foster, PS; Tay, HL; Oliver, BG

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

Foster, PS Tay, HL Oliver, BG

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Publisher:: AMER SOC CLINICAL INVESTIGATION INC
Publication Type:: Journal Article
Citation:: J Clin Invest, 2022, 132, (11), pp. e160595
Issue Date:: 2022-06-01

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Field	Value	Language
dc.contributor.author	Foster, PS
dc.contributor.author	Tay, HL
dc.contributor.author	Oliver, BG
dc.date.accessioned	2023-01-31T02:26:38Z
dc.date.available	2023-01-31T02:26:38Z
dc.date.issued	2022-06-01
dc.identifier.citation	J Clin Invest, 2022, 132, (11), pp. e160595
dc.identifier.issn	0021-9738
dc.identifier.issn	1558-8238
dc.identifier.uri	http://hdl.handle.net/10453/165647
dc.description.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.
dc.format	Print
dc.language	eng
dc.publisher	AMER SOC CLINICAL INVESTIGATION INC
dc.relation.ispartof	J Clin Invest
dc.relation.isbasedon	10.1172/JCI160595
dc.rights	info:eu-repo/semantics/restrictedAccess
dc.rights	Copyright: © 2022, Foster et al. This is an open access article published under the terms of the Creative Commons Attribution 4.0 International License.
dc.subject	11 Medical and Health Sciences
dc.subject.classification	Immunology
dc.subject.mesh	Alveolar Epithelial Cells
dc.subject.mesh	Carrier Proteins
dc.subject.mesh	Cation Transport Proteins
dc.subject.mesh	Humans
dc.subject.mesh	Idiopathic Pulmonary Fibrosis
dc.subject.mesh	Lung
dc.subject.mesh	Sirtuin 1
dc.subject.mesh	Lung
dc.subject.mesh	Humans
dc.subject.mesh	Carrier Proteins
dc.subject.mesh	Cation Transport Proteins
dc.subject.mesh	Idiopathic Pulmonary Fibrosis
dc.subject.mesh	Sirtuin 1
dc.subject.mesh	Alveolar Epithelial Cells
dc.title	Deficiency in the zinc transporter ZIP8 impairs epithelia renewal and enhances lung fibrosis.
dc.type	Journal Article
utslib.citation.volume	132
utslib.location.activity	United States
utslib.for	11 Medical and Health Sciences
pubs.organisational-group	/University of Technology Sydney
pubs.organisational-group	/University of Technology Sydney/Faculty of Science
pubs.organisational-group	/University of Technology Sydney/Strength - CHT - Health Technologies
pubs.organisational-group	/University of Technology Sydney/Faculty of Science/School of Life Sciences
pubs.organisational-group	/University of Technology Sydney/Centre for Health Technologies (CHT)
utslib.copyright.status	recently_added	*
dc.date.updated	2023-01-31T02:26:34Z
pubs.issue	11
pubs.publication-status	Published
pubs.volume	132
utslib.citation.issue	11

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.

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http://hdl.handle.net/10453/165647