Evidence map›Paper›PMID 24920662›Full record

ArticleScience translational medicine2014

Chitinase 3-like 1 suppresses injury and promotes fibroproliferative responses in Mammalian lung fibrosis.

Yang Zhou, Hong Peng, Huanxing Sun, Xueyan Peng, Chuyan Tang, Ye Gan, Xiaosong Chen, Aditi Mathur, Buqu Hu, Martin D Slade and 10 more

Abstract read
In one paragraph

Article in Science translational medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 139 papers.

0numbers the graph read from it
0cells of the map it votes in
139citing papers in PubMed
6.0field-weighted citation impact, top 3% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

139 citing papers in PubMed, 217 citations in OpenAlex.

  1. Kidney Biomarkers of Injury and Repair as Predictors of Contrast-Associated AKI: A Substudy of the PRESERVE Trial.American journal of kidney diseases : the official journal of the National Kidney Foundation · 2020
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  9. Loss ofbioRxiv : the preprint server for biology · 2026
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79 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

20 authors at 2 institutions in 1 country.

Yang Zhou *Section of Pulmonary, Critical Care and Sleep Medicine, Department of Medicine, Yale School of Medicine, New Haven, CT 06520, USA.
Hong Peng *Department of Respiratory Medicine, The Second Xiangya Hospital of Central South University, Changsha, Hunan 410011, PR China.
Huanxing Sun *Section of Pulmonary, Critical Care and Sleep Medicine, Department of Medicine, Yale School of Medicine, New Haven, CT 06520, USA.
Xueyan PengSection of Pulmonary, Critical Care and Sleep Medicine, Department of Medicine, Yale School of Medicine, New Haven, CT 06520, USA.
Chuyan TangSection of Pulmonary, Critical Care and Sleep Medicine, Department of Medicine, Yale School of Medicine, New Haven, CT 06520, USA.
Ye GanSection of Pulmonary, Critical Care and Sleep Medicine, Department of Medicine, Yale School of Medicine, New Haven, CT 06520, USA.
Xiaosong ChenSection of Pulmonary, Critical Care and Sleep Medicine, Department of Medicine, Yale School of Medicine, New Haven, CT 06520, USA.
Aditi MathurSection of Pulmonary, Critical Care and Sleep Medicine, Department of Medicine, Yale School of Medicine, New Haven, CT 06520, USA.
Buqu HuSection of Pulmonary, Critical Care and Sleep Medicine, Department of Medicine, Yale School of Medicine, New Haven, CT 06520, USA.
Martin D SladeSection of Pulmonary, Critical Care and Sleep Medicine, Department of Medicine, Yale School of Medicine, New Haven, CT 06520, USA.
Ruth R MontgomeryProgram on Aging, Yale School of Medicine, New Haven, CT 06520, USA.
Albert C ShawProgram on Aging, Yale School of Medicine, New Haven, CT 06520, USA.
Robert J HomerDepartment of Pathology, Yale School of Medicine, New Haven, CT 06520, USA.
Eric S WhiteDepartment of Medicine, University of Michigan School of Medicine, Ann Arbor, MI 48109, USA.
Chang-Min LeeSection of Pulmonary, Critical Care and Sleep Medicine, Department of Medicine, Yale School of Medicine, New Haven, CT 06520, USA.
Meagan W MooreSection of Pulmonary, Critical Care and Sleep Medicine, Department of Medicine, Yale School of Medicine, New Haven, CT 06520, USA.
Mridu GulatiSection of Pulmonary, Critical Care and Sleep Medicine, Department of Medicine, Yale School of Medicine, New Haven, CT 06520, USA.
Chun Geun LeeSection of Pulmonary, Critical Care and Sleep Medicine, Department of Medicine, Yale School of Medicine, New Haven, CT 06520, USA.
Jack A EliasDivision of Biology and Medicine, Warren Alpert School of Medicine at Brown University, Providence, RI 02912, USA.
Erica L HerzogSection of Pulmonary, Critical Care and Sleep Medicine, Department of Medicine, Yale School of Medicine, New Haven, CT 06520, USA.
University of Michigan–Ann Arbor · USYale University · US

Funding

Yale University Clinical and Translational Science Award ProgramUL1TR000142 · NCATS · YALE UNIVERSITY · PI SHERWIN, ROBERT S · 2012 to 2015
$31.8M
Respiratory Computational Discovery CoreP01HL114501 · NHLBI · WEILL MEDICAL COLL OF CORNELL UNIV · PI SILVERMAN, EDWIN K · 2013 to 2025
$24.9M
PULMONARY CELLULAR AND MOLECULAR BIOLOGY TRAININGT32HL007749 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Robert Pickett Dickson · 1993 to 2026
$19.9M
Novel Immunologic Effects of Semaphorin 7a in IPFR01HL109233 · NHLBI · YALE UNIVERSITY · PI HERZOG, ERICA L · 2011 to 2019
$3.7M
Matrix and Bioreactors for Human Lung RegenerationU01HL111016 · NHLBI · YALE UNIVERSITY · PI NIKLASON, LAURA E, WHITE, ERIC S · 2012 to 2016
$3.2M
YKL-40 in Idiopathic Pulmonary Fibrosis and Kidney TransplantationU01HL108638 · NHLBI · YALE UNIVERSITY · PI ELIAS, JACK A · 2011 to 2014
$2.6M
Role of EIIIA fibronectin in pulmonary fibrosisR01HL085083 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI WHITE, ERIC S · 2007 to 2011
$1.9M
Matrix biomarkers and compartmentalization in IPFR01HL109118 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI WHITE, ERIC S · 2012 to 2015
$1.8M
Midcareer Award in Translational Immunology of AgingK24AG042489 · NIA · YALE UNIVERSITY · PI SHAW, ALBERT C · 2012 to 2022
$1.8M
BRP-39/YKL-40 in Th2 Inflammation and AsthmaR01HL093017 · NHLBI · YALE UNIVERSITY · PI ELIAS, JACK A · 2010 to 2013
$1.6M
Significance Circulating Semaphorin 7a+ve Cells in Pulmonary SarcoidosisU01HL112702 · NHLBI · YALE UNIVERSITY · PI HERZOG, ERICA L · 2012 to 2014
$488k
NCATS NIH HHS UL1 TR000142NHLBI NIH HHS 5U01HL112702NHLBI NIH HHS HL093017NHLBI NIH HHS HL109033NHLBI NIH HHS P01 HL114501NHLBI NIH HHS R01 HL085083NHLBI NIH HHS R01 HL093017NHLBI NIH HHS R01 HL109118NHLBI NIH HHS R01 HL109233NHLBI NIH HHS T32 HL007749NHLBI NIH HHS U01 HL108638NHLBI NIH HHS U01HL108638NHLBI NIH HHS U01HL109118NHLBI NIH HHS U01 HL111016NHLBI NIH HHS U01 HL112702NIA NIH HHS K24 AG042489PHS HHS N01-HHS N272201100019C
6 · The paper itself

Abstract

Epithelial injury, alternative macrophage accumulation, and fibroproliferation coexist in the lungs of patients with idiopathic pulmonary fibrosis (IPF). Chitinase 3-like 1 (CHI3L1) is a prototypic chitinase-like protein that has been retained over species and evolutionary time. However, the regulation of CHI3L1 in IPF and its ability to regulate injury and/or fibroproliferative repair have not been fully defined. We demonstrated that CHI3L1 levels were elevated in patients with IPF. High levels of CHI3L1 are associated with progression--as defined by lung transplantation or death--and with scavenger receptor-expressing circulating monocytes in an ambulatory IPF population. In preterminal acute exacerbations of IPF, CHI3L1 levels were reduced and associated with increased levels of apoptosis. We also demonstrated that in bleomycin-treated mice, CHI3L1 expression was acutely and transiently decreased during the injury phase and returned toward and eventually exceeded baseline levels during the fibrotic phase. In this model, CHI3L1 played a protective role in injury by ameliorating inflammation and cell death, and a profibrotic role in the repair phase by augmenting alternative macrophage activation, fibroblast proliferation, and matrix deposition. Using three-dimensional culture system of a human fibroblast cell line, we found that CHI3L1 is sufficient to induce low grade myofibroblast transformation. In combination, these studies demonstrate that CHI3L1 is stimulated in IPF, where it represents an attempt to diminish injury and induce repair. They also demonstrate that high levels of CHI3L1 are associated with disease progression in ambulatory patients and that a failure of the CHI3L1 antiapoptotic response might contribute to preterminal disease exacerbations.

Indexed as

AdipokinesAnimalsApoptosisBone Marrow TransplantationCell ProliferationChitinase-3-Like Protein 1Enzyme-Linked Immunosorbent AssayFemaleFibroblastsFlow CytometryHumansIn Situ Nick-End LabelingLectinsLungMiceMice, KnockoutAdipokinesCHI3L1 protein, humanChitinase-3-Like Protein 1Lectins

Identifiers

PMID24920662
PMCPMC4340473
OpenAlexW2159203930

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.