Evidence map›Paper›PMID 29567123›Full record

ReviewMatrix biology : journal of the International Society for Matrix Biology2018

Fibrosis: Lessons from OMICS analyses of the human lung.

Guoying Yu, Gabriel H Ibarra, Naftali Kaminski

Abstract readReview
In one paragraph

Review in Matrix biology : journal of the International Society for Matrix Biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
–field-weighted citation impact
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

32 citing papers in PubMed.

  1. Altered Metabolism in Idiopathic Pulmonary Fibrosis.Journal of cellular physiology · 2025
    Review
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  16. Toll-Interacting Protein in Pulmonary Diseases. Abiding by the Goldilocks Principle.American journal of respiratory cell and molecular biology · 2021
    Review
  17. Mouse Models of Lung Fibrosis.Methods in molecular biology (Clifton, N.J.) · 2021
    Article
  18. Review
  19. Chaotic activation of developmental signalling pathways drives idiopathic pulmonary fibrosis.European respiratory review : an official journal of the European Respiratory Society · 2020
    Review
  20. The Idiopathic Pulmonary Fibrosis Cell Atlas.American journal of physiology. Lung cellular and molecular physiology · 2020
    Article
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

3 authors.

Guoying YuSection of Pulmonary, Critical Care and Sleep Medicine, Department of Internal Medicine, Yale University School of Medicine, United States.
Gabriel H IbarraSection of Pulmonary, Critical Care and Sleep Medicine, Department of Internal Medicine, Yale University School of Medicine, United States.
Naftali KaminskiSection of Pulmonary, Critical Care and Sleep Medicine, Department of Internal Medicine, Yale University School of Medicine, United States. Electronic address: naftali.kaminski@yale.edu.

Funding

Genomic Analysis of Tissue and Cellular Heterogeneity in IPFR01HL127349 · NHLBI · YALE UNIVERSITY · PI BENOS, PANAGIOTIS V, KAMINSKI, NAFTALI · 2015 to 2025
$5.9M
Mir-29 mimicry as a therapy for pulmonary fibrosisUH3HL123886 · NHLBI · YALE UNIVERSITY · PI KAMINSKI, NAFTALI · 2016 to 2018
$4.5M
Alveolar DevMAPU01HL122626 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI AMBALAVANAN, NAMASIVAYAM, HAGOOD, JAMES S. · 2014 to 2018
$3.7M
Molecular Phenotypes within and across disease boundaries in IPF and COPDR01HL095397 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI KAMINSKI, NAFTALI, SHAPIRO, STEVEN D · 2008 to 2011
$3.0M
NHLBI NIH HHS R01 HL095397NHLBI NIH HHS R01 HL127349NHLBI NIH HHS U01 HL122626NHLBI NIH HHS UH3 HL123886
6 · The paper itself

Abstract

In recent decades there has been a significant shift in our understanding of idiopathic pulmonary fibrosis (IPF), a progressive and lethal disorder. While initially much of the mechanistic understanding was derived from hypotheses generated from animal models of disease, in recent decades new insights derived from humans with IPF have taken precedence. This is mainly because of the establishment of large collections of IPF lung tissues and patient cohorts, and the emergence of high throughput profiling technologies collectively termed 'omics' technologies based on their shared suffix. In this review we describe impacts of 'omics' analyses of human IPF samples on our understanding of the disease. In particular, we discuss the results of genomics and transcriptomics studies, as well as proteomics, epigenomics and metabolomics. We then describe how these findings can be integrated in a modified paradigm of human idiopathic pulmonary fibrosis, that introduces the 'hallmarks of aging' as a central theme in the IPF lung. This allows resolution of all the disparate cellular and molecular features in IPF, from the central role of epithelial cells, through the dramatic phenotypic alterations observed in fibroblasts and the numerous aberrations that inflammatory cells exhibit. We end with reiterating a call for renewed efforts to collect and analyze carefully characterized human tissues, in ways that would facilitate implementation of novel technologies for high resolution single cell omics profiling.

Indexed as

Gene Regulatory NetworksComputational BiologyEpigenomicsGene Expression ProfilingGene Expression RegulationGenomicsHumansIdiopathic Pulmonary FibrosisLungMetabolomicsProteomicsGenomicsMicrobiomeMitochondriaPulmonary fibrosisSenescenceTelomereTranscriptomics

Identifiers

PMID29567123
PMCPMC6015529

What OpenQuestion holds

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Registered trials

None linked

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.